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Journal articles on the topic 'High mobility group phosphoprotein A2'

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Published: 4 June 2021

Last updated: 20 February 2023

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1

Natarajan, Suchitra, Farhana Begum, Jeonga Gim, Landon Wark, Dana Henderson, James R. Davie, Sabine Hombach-Klonisch, and Thomas Klonisch. "High Mobility Group A2 protects cancer cells against telomere dysfunction." Oncotarget 7, no. 11 (January 18, 2016): 12761–82. http://dx.doi.org/10.18632/oncotarget.6938.

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2

Li, A. Y. J., H. H. Lin, C. Y. Kuo, H. M. Shih, C. C. C. Wang, Y. Yen, and D. K. Ann. "High-Mobility Group A2 Protein Modulates hTERT Transcription To Promote Tumorigenesis." Molecular and Cellular Biology 31, no. 13 (May 2, 2011): 2605–17. http://dx.doi.org/10.1128/mcb.05447-11.

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3

Wang, Ya-Dong, Jia-Ding Mao, Jun-Feng Wang, and Mao-Qi Xu. "MiR-590 Suppresses Proliferation and Induces Apoptosis in Pancreatic Cancer by Targeting High Mobility Group A2." Technology in Cancer Research & Treatment 19 (January 1, 2020): 153303382092814. http://dx.doi.org/10.1177/1533033820928143.

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Background: Pancreatic ductal adenocarcinoma is a common malignancy with high morbidity. MicroRNAs have been demonstrated to be critical posttranscriptional regulators in tumorigenesis. This study aimed to investigate the effect of microRNA-590 on the proliferation and apoptosis of pancreatic ductal adenocarcinoma. Material and Methods: The expression of microRNA-590 and high mobility group AT-hook 2 were examined in clinical pancreatic ductal adenocarcinoma tissues. Pancreatic ductal adenocarcinoma cell line Capan-2 was employed and transfected with microRNA-590 mimics or inhibitor. The correlation between microRNA-590 and high mobility group AT-hook 2 was verified by luciferase reporter assay. Cell viability and apoptosis were detected by MTT and flow cytometry assay. The protein level of high mobility group AT-hook 2, AKT, p-AKT, mTOR, and phosphorylated mTOR were analyzed by Western blotting. Results: MicroRNA-590 was found to be negatively correlated with the expression of high mobility group AT-hook 2 in pancreatic ductal adenocarcinoma tissues. Further studies identified high mobility group AT-hook 2 as a direct target of microRNA-590. Moreover, overexpression of microRNA-590 downregulated expression of high mobility group AT-hook 2, reduced cell viability, and promoted cell apoptosis, while knockdown of miR-590 led to an inverse result. MicroRNA-590 also suppressed the phosphorylation of AKT and mTOR without altering total AKT and mTOR levels. Conclusion: Our study indicated that microRNA-590 negatively regulates the expression of high mobility group AT-hook 2 in clinical specimens and in vitro. MicroRNA-590 can inhibit cell proliferation and induce cell apoptosis in pancreatic ductal adenocarcinoma cells. This regulatory effect of microRNA-590 may be associated with AKT signaling pathway. Therefore, microRNA-590 has the potential to be used as a biomarker for predicting the progression of pancreatic ductal adenocarcinoma.

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4

Hawsawi, Ohuod, Veronica Henderson, Liza J. Burton, Jodi Dougan, Peri Nagappan, and Valerie Odero-Marah. "High mobility group A2 (HMGA2) promotes EMT via MAPK pathway in prostate cancer." Biochemical and Biophysical Research Communications 504, no. 1 (September 2018): 196–202. http://dx.doi.org/10.1016/j.bbrc.2018.08.155.

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5

Gong, Jian, Yuxiang Wang, Buping Jiang, Bin Xu, and Chuanzhen Hu. "Impact of high-mobility-group A2 overexpression on epithelial-mesenchymal transition in pancreatic cancer." Cancer Management and Research Volume 11 (May 2019): 4075–84. http://dx.doi.org/10.2147/cmar.s199289.

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6

Cui, Tengjiao, Suzanne Joynt, Victor Morillo, Maria Baez, Zhichun Hua, Xiaotang Wang, and Fenfei Leng. "Large Scale Preparation of the Mammalian High Mobility Group Protein A2 for Biophysical Studies." Protein & Peptide Letters 14, no. 1 (January 1, 2007): 87–91. http://dx.doi.org/10.2174/092986607779117281.

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7

Gong, Yan, Xin Jin, Quan-Shun Wang, Shi-Hui Wei, Bao-Ke Hou, Hong-Yang Li, Mao-Nian Zhang, and Zhao-Hui Li. "The involvement of high mobility group 1 cytokine and phospholipases A2 in diabetic retinopathy." Lipids in Health and Disease 13, no. 1 (2014): 156. http://dx.doi.org/10.1186/1476-511x-13-156.

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8

Heilmann, Thorsten, Florian Vondung, Christoph Borzikowsky, Sandra Krüger, Mohamed Elessawy, Ibrahim Alkatout, Antonia Wenners, et al. "Cytoplasmic levels of high mobility group A2 determine survival prognoses in breast cancer patients." International Journal of Biological Markers 35, no. 2 (May 12, 2020): 20–28. http://dx.doi.org/10.1177/1724600820917990.

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Background: High mobility group A proteins are involved in chromatin remodeling, thereby influencing multiple fundamental biological processes. HMGA2 has been linked to oncogenic traits among a variety of malignancies. Objective: To determine the prognostic implications of subcellular distribution patterns of HMGA2 in breast cancer. Methods: Nuclear and cytoplasmic HMGA2 was evaluated in 342 breast cancer specimens and matched with clinico-pathological parameters. Results: Overall and cytoplasmic, but not nuclear, levels of HMGA2 correlated with better survival prognoses in our collective (hazard ratio (HR) 0.34, P = 0.001 and HR 0.34, P < 0.001, respectively). The protective effect of cytoplasmic HMGA2 persisted in the Luminal A and triple negative breast cancer subgroups. Evaluating Luminal A and B subgroups jointly, only cytoplasmic, but not overall or nuclear HMGA2 levels were associated with better survival (HR 0.42, 95% confidence interval 0.21, 0.86, P = 0.017), irrespective of tumor size and node status. The addition of HMGA2 overall and cytoplasmic scores strengthened the prognostic selectivity in a model of conventional breast cancer risk factors. No predictive significance with regard to endocrine or chemoendocrine therapies was observed. Conclusion: Unexpectedly, we found a favorable survival probability upon overall levels of HMGA2 in our breast cancer collective, which was predominantly determined by the presence of HMGA2 in the cytoplasm.

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9

Binabaj, Maryam Moradi, Atena Soleimani, Farzad Rahmani, Amir Avan, Majid Khazaei, Hamid Fiuji, Saman Soleimanpour, et al. "Prognostic value of high mobility group protein A2 (HMGA2) over-expression in cancer progression." Gene 706 (July 2019): 131–39. http://dx.doi.org/10.1016/j.gene.2019.04.088.

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10

Peng, Yi, Jordan Laser, Guizhi Shi, Khush Mittal, Jonathan Melamed, Peng Lee, and Jian-Jun Wei. "Antiproliferative Effects by Let-7 Repression of High-Mobility Group A2 in Uterine Leiomyoma." Molecular Cancer Research 6, no. 4 (April 2008): 663–73. http://dx.doi.org/10.1158/1541-7786.mcr-07-0370.

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11

Liu, Zhuoxing, Kunpeng Wu, Zhixiong Yang, and Aibing Wu. "High-mobility group A2 overexpression is an unfavorable prognostic biomarker for nasopharyngeal carcinoma patients." Molecular and Cellular Biochemistry 409, no. 1-2 (July 17, 2015): 155–62. http://dx.doi.org/10.1007/s11010-015-2521-0.

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12

Chen, Hwudaurw, Earlphia Sells, Ritu Pandey, Edward R. Abril, Chiu-Hsieh Hsu, Robert S. Krouse, Raymond B. Nagle, Georgios Pampalakis, Georgia Sotiropoulou, and Natalia A. Ignatenko. "Kallikrein 6 protease advances colon tumorigenesis via induction of the high mobility group A2 protein." Oncotarget 10, no. 58 (October 22, 2019): 6062–78. http://dx.doi.org/10.18632/oncotarget.27153.

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13

Venkatesan, Nalini, Mallikarjuna Kandalam, Gunisha Pasricha, Venil Sumantran, Guidalberto Manfioletti, Santa Jeremy Ono, Maddy Ashwin Reddy, and Subramanian Krishnakumar. "Expression of High Mobility Group A2 Protein in Retinoblastoma and its Association With Clinicopathologic Features." Journal of Pediatric Hematology/Oncology 31, no. 3 (March 2009): 209–14. http://dx.doi.org/10.1097/mph.0b013e318197978d.

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14

Nie, Dan, Lingping Zhang, Qian Guo, and Xiguang Mao. "High mobility group protein A2 overexpression indicates poor prognosis for cancer patients: a meta-analysis." Oncotarget 9, no. 1 (December 10, 2017): 1237–47. http://dx.doi.org/10.18632/oncotarget.23085.

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15

Wei, Chun-Hui. "Effect of silencing of high mobility group A2 gene on gastric cancer MKN-45 cells." World Journal of Gastroenterology 19, no. 8 (2013): 1239. http://dx.doi.org/10.3748/wjg.v19.i8.1239.

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16

Fusco, Ileana, Deepak Babu, Simona Mellone, Nadia Barizzone, Flavia Prodam, Antonella Fanelli, Ranjit Muniswamy, et al. "Variations in the high-mobility group-A2 gene (HMGA2) are associated with idiopathic short stature." Pediatric Research 79, no. 2 (November 4, 2015): 258–61. http://dx.doi.org/10.1038/pr.2015.225.

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17

Wang, Lihui, Weiming Weng, Shuhui Yang, Shasha Yang, and Richang Du. "Circle RNA circ_0007331 promotes colorectal carcinoma by targeting miR-205-5p/high-mobility group A2 axis." Bioengineered 13, no. 4 (April 1, 2022): 9312–21. http://dx.doi.org/10.1080/21655979.2022.2051857.

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18

Zhu, Shoukang, Shanming Deng, Qi Ma, Taifang Zhang, Chunling Jia, Degen Zhuo, Falin Yang, et al. "MicroRNA-10A* and MicroRNA-21 Modulate Endothelial Progenitor Cell Senescence Via Suppressing High-Mobility Group A2." Circulation Research 112, no. 1 (January 4, 2013): 152–64. http://dx.doi.org/10.1161/circresaha.112.280016.

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19

Bouatia-Naji, Nabila, Marion Marchand, Christine Cavalcanti-Proença, Samia Daghmoun, Emmanuelle Durand, Jean Tichet, Michel Marre, Beverley Balkau, Philippe Froguel, and Claire Lévy-Marchal. "Smallness for gestational age interacts with high mobility group A2 gene genetic variation to modulate height." European Journal of Endocrinology 160, no. 4 (April 2009): 557–60. http://dx.doi.org/10.1530/eje-08-0794.

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ObjectiveHeight variability is largely under genetic control, although identifying the genetic variants involved has been until recently challenging. Smallness for gestational age (SGA) is a risk factor for adult short stature. Genome-wide association studies have identified a single nucleotide polymorphism (SNP) (rs1042725) in the high mobility group A2 gene (HMGA2) that consistently associates with height variability but its interaction with SGA is unknown.DesignWe assess the contribution of rs1042725 SNP and height variability in a French population and the impact of rs1042725 on SGA status at birth and height at adulthood in SGA individuals.MethodsWe genotyped rs1042725 in 4710 healthy participants from the Data from an Epidemiological Study on the Insulin Resistance syndrome (DESIR) cohort, 743 normal birth weight and 660 SGA individuals from the Haguenau study.Resultsrs1042725 is associated with increased height in the cohort participants (0.36 cm 95% CI (0.12–0.61) per C allele, P=0.004) but not with the SGA status or birth length. Interestingly, rs1042725 had a stronger effect on height in SGA participants (0.94 cm 95% CI (0.24–1.64) per C allele, P=0.009), especially in men (1.45 cm 95% CI (0.44–2.46) per C allele, P=0.005) in whom rs1042725 may explain 3% of height variability. SGA men carrying at least one C allele copy experienced more frequent catch-up in height (Padd=0.07; Pdom=0.03).ConclusionsOur study supports further the contribution of HMGA2 rs1042725 to height variability in European populations and shows an increased effect on height in SGA individuals where this variant favors height catch-up.

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20

Tan, E.-Jean, Kaoru Kahata, Oskar Idås, Sylvie Thuault, Carl-Henrik Heldin, and Aristidis Moustakas. "The high mobility group A2 protein epigenetically silences the Cdh1 gene during epithelial-to-mesenchymal transition." Nucleic Acids Research 43, no. 1 (December 9, 2014): 162–78. http://dx.doi.org/10.1093/nar/gku1293.

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21

Bakhidze, E. V., A. V. Malek, and A. V. Belyaeva. "The target genes research for diagnosis, therapy and prognosis in cases with ovarian cancer." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 16060. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.16060.

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16060 Background: Epithelial ovarian cancer has one of the worst prognoses among gynecologic malignancies. Molecular genetic analyses of ovarian cancers have uncovered genetic alterations of several genes. Normal tissues were readily distinguished from tumor tissues. These studies identified several genes, such as High mobility group A2 (HMG A2) proteins. The expression of HMG A2 gene is detected in foetal stage of human development and stopped in normal adult tissues. Elevation of the HMG A2 gene expression was shown for several human malignant tumours. Targeted supression of HMG A2 protein synthesis can be one of important directions for anti-tumour therapy in cases of ovarian cancer Methods: The HMG A2 gene expression was searched in 48 flash-frozen samples of ovarian serous papillary adenocarcinoma and 12 samples of normal ovarian tissue. The HMG A2 gene expression was investigated by RNA in situ hybridisation. Results: High and middle level of HMG A2 gene expression was shown in 37 from 48 (77%) ovarian cancer samples. HMG A2 mRNA was not detected in normal ovarian surface epithelium. Low grade tumour differentiation (G3) was detected in 24 cases from 37 (64,9%), middle differentiation (G2) was detected in 12 cases (32,4%) and high grade differentiation (G1) was detected in 1 case (2,7%). Conclusions: HMG A2 high expression is a typical and important feature of serouse type of ovarian carcinoma. High level of HMG A2 gene expression correlate with low grade tumour differentiation. No significant financial relationships to disclose.

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22

LEE, JUNHYUN, SHINJUNG HA, CHAN-KWON JUNG, and HAN HONG LEE. "High-mobility-group A2 overexpression provokes a poor prognosis of gastric cancer through the epithelial-mesenchymal transition." International Journal of Oncology 46, no. 6 (April 1, 2015): 2431–38. http://dx.doi.org/10.3892/ijo.2015.2947.

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23

Chung, Jaewook, Xia Zhang, Bruce Collins, Renan B. Sper, Katherine Gleason, Sean Simpson, Sehwon Koh, et al. "High mobility group A2 (HMGA2) deficiency in pigs leads to dwarfism, abnormal fetal resource allocation, and cryptorchidism." Proceedings of the National Academy of Sciences 115, no. 21 (May 7, 2018): 5420–25. http://dx.doi.org/10.1073/pnas.1721630115.

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Expression of HMGA2 is strongly associated with body size and growth in mice and humans. In mice, inactivation of one or both alleles of Hmga2 results in body-size reductions of 20% and 60%, respectively. In humans, microdeletions involving the HMGA2 locus result in short stature, suggesting the function of the HMGA2 protein is conserved among mammals. To test this hypothesis, we generated HMGA2-deficient pigs via gene editing and somatic cell nuclear transfer (SCNT). Examination of growth parameters revealed that HMGA2−/+ male and female pigs were on average 20% lighter and smaller than HMGA2+/+ matched controls (P < 0.05). HMGA2−/− boars showed significant size reduction ranging from 35 to 85% of controls depending on age (P < 0.05), and organ weights were also affected (P < 0.05). HMGA2−/+ gilts and boars exhibited normal reproductive development and fertility, while HMGA2−/− boars were sterile due to undescended testes (cryptorchidism). Crossbreeding HMGA2−/+ boars and gilts produced litters lacking the HMGA2−/− genotype. However, analysis of day (D) D40 and D78 pregnancies indicated that HMGA2−/− fetuses were present at the expected Mendelian ratio, but placental abnormalities were seen in the D78 HMGA2−/− concepti. Additionally, HMGA2−/− embryos generated by gene editing and SCNT produced multiple pregnancies and viable offspring, indicating that lack of HMGA2 is not lethal per se. Overall, our results show that the effect of HMGA2 with respect to growth regulation is highly conserved among mammals and opens up the possibility of regulating body and organ size in a variety of mammalian species including food and companion animals.

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24

Abe, N., T. Watanabe, Y. Suzuki, N. Matsumoto, T. Masaki, T. Mori, M. Sugiyama, G. Chiappetta, A. Fusco, and Y. Atomi. "An increased high-mobility group A2 expression level is associated with malignant phenotype in pancreatic exocrine tissue." British Journal of Cancer 89, no. 11 (November 25, 2003): 2104–9. http://dx.doi.org/10.1038/sj.bjc.6601391.

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25

Natarajan, Suchitra, Thatchawan Thanasupawat, Amy Rommel, Hugo Bergen, Inder Verma, Marc Del Bigio, Marshall Pitz, et al. "Targeting oncofetal high mobility group A2 (HMGA2) to increase sensitivity to temozolomide (TMZ) in glioblastoma (GB) cells." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 41, s2 (October 2014): S3—S4. http://dx.doi.org/10.1017/cjn.2014.52.

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26

Kim, Tae Hoen, Ji-ye Song, Hyun Park, Ju-yeon Jeong, A.-young Kwon, Jin Hyung Heo, Haeyoun Kang, Gwangil Kim, and Hee Jung An. "miR-145, targeting high-mobility group A2, is a powerful predictor of patient outcome in ovarian carcinoma." Cancer Letters 356, no. 2 (January 2015): 937–45. http://dx.doi.org/10.1016/j.canlet.2014.11.011.

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27

Gallivan, Monica V., Laura A. Worfolk, Christina D. Lapuz, Olivia Saqui, Larielyn P. Pan, and Jeffrey S. Dlott. "Comparison of High Resolution HPLC with Capillary Zone Electrophoresis in Hemoglobin A2 Measurement." Blood 110, no. 11 (November 16, 2007): 3832. http://dx.doi.org/10.1182/blood.v110.11.3832.3832.

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Abstract With the advent of high performance liquid chromatography (HPLC) accurate and precise measurement of hemoglobin A2 has been available for over 20 years. When microcytosis is present an elevated A2 is used as a surrogate marker for identification of beta thalassemia carriers. This combination is a very useful screening test. In contrast, A2 measurement in the low range is used to a lesser extent in screening for alpha thalassemia, delta chain variants and delta thalassemia. In the absence of structural variants A2 measurement by HPLC is accurate in the normal, high, and low ranges. This accuracy however does not hold true when samples harbor structural variants, particularly in the presence of Hb S as there are glycated and degraded fractions of S that co-elute with A2, thus falsely elevating the A2 value. In addition, with E and “D” type variants there is no A2 result or a falsely decreased value because A2 partially or completely co-elutes with the variant. In contrast to HPLC, capillary zone electrophoresis (CZE) separates the hemoglobin fractions according to their electrophoretic mobility with an alkaline buffer. We compared HbA2 measurement by high resolution (HR) HPLC (Primus Diagnostics) and CZE (Sebia CapillaryS) in samples without structural variants in the normal, high, and low ranges and in samples containing common structural variants. The 112 normals were from healthy, hematologically normal adult volunteers. The 20 samples in the high A2 range did not include structural variants and all had microcytosis. The 42 low A2 samples were from individuals without microcytosis in whom isoelectricfocusing (IEF) was also performed to identify delta chain variants. The heterozygotes for S, C, E and “D” had adult phenotypes and based on the percentages of the variant did not appear to have alpha thalassemia. In the “D” group there were 6 D-Punjab, 1 Osu-Christiansburg, and 1 Korle-Bu. G-Philadelphia was excluded as it occurs in association with alpha thalassemia. The results of our comparison study are shown in Table I. Besides what is indicated in the table we identified 9 individuals in the low A2 group that had delta chain variants identified on CZE but silent on HR-HPLC. These delta variants were confirmed by IEF. In summary, in the absence of structural variants these data indicate excellent correlation between HR-HPLC and CZE in the normal, high and low A2 ranges. In the low A2 range CZE has an added advantage over HR-HPLC in detecting delta variants. In the C-Trait group both methodologies appear equivalent but as expected in the S-Trait, E-Trait, and “D” Trait groups the CZE value appears to be more accurate. Compared to the normal group, however, there is a slight positive bias in S-Trait and E-Trait. In conclusion both methodologies appear complementary and can be used in combination for greater accuracy in hemoglobin identification and quantification of fractions. Table I Parameter N HR-HPLC Mean HR-HPLC 1 SD CZE Mean CZE 1 SD y R value Normal range A2 (1.8–3.5) 112 2.6 0.17 2.6 0.15 1.02 0.90 High range A2 > 3.6 20 5.1 0.59 5.0 0.5 0.98 0.94 Low range A <1.8 42 1.4 0.25 1.5 0.29 1.08 0.91 S Trait 32 4.0 0.25 3.1 0.18 0.76 0.66 C trait 15 3.1 0.28 3.1 0.3 0.98 0.66 E Trait 12 2.0 0.55 3.4 0.41 1.52 0.38 “D” Trait 8 N/A N/A 2.9 0.18 N/A N/A

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28

Galdiero, Francesca, Annunciata Romano, Rosa Pasquinelli, Sandro Pignata, Stefano Greggi, Emilia Vuttariello, Anna Maria Bello, et al. "Detection of high mobility group A2 specific mRNA in the plasma of patients affected by epithelial ovarian cancer." Oncotarget 6, no. 22 (February 12, 2015): 19328–35. http://dx.doi.org/10.18632/oncotarget.2896.

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29

Guo, Xiangjun, Jiaxin Shi, Yan Wen, Mengmeng Li, Qin Li, Xiaomei Li, and Jiashu Li. "Increased high-mobility group A2 correlates with lymph node metastasis and prognosis of non-small cell lung cancer." Cancer Biomarkers 21, no. 3 (February 14, 2018): 547–55. http://dx.doi.org/10.3233/cbm-170401.

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30

Lee, Seunghee, Ji-Won Jung, Sang-Bum Park, Kyounghwan Roh, Su Yeon Lee, Ju Han Kim, Soo-Kyung Kang, and Kyung-Sun Kang. "Histone deacetylase regulates high mobility group A2-targeting microRNAs in human cord blood-derived multipotent stem cell aging." Cellular and Molecular Life Sciences 68, no. 2 (July 21, 2010): 325–36. http://dx.doi.org/10.1007/s00018-010-0457-9.

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31

Di Agostino, Silvia, Monica Fedele, Paolo Chieffi, Alfredo Fusco, Pellegrino Rossi, Raffaele Geremia, and Claudio Sette. "Phosphorylation of High-Mobility Group Protein A2 by Nek2 Kinase during the First Meiotic Division in Mouse Spermatocytes." Molecular Biology of the Cell 15, no. 3 (March 2004): 1224–32. http://dx.doi.org/10.1091/mbc.e03-09-0638.

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The mitogen-activated protein kinase (MAPK) pathway is required for maintaining the chromatin condensed during the two meiotic divisions and to avoid a second round of DNA duplication. However, molecular targets of the MAPK pathway on chromatin have not yet been identified. Here, we show that the architectural chromatin protein HMGA2 is highly expressed in male meiotic cells. Furthermore, Nek2, a serine-threonine kinase activated by the MAPK pathway in mouse pachytene spermatocytes, directly interacts with HMGA2 in vitro and in mouse spermatocytes. The interaction does not depend on the activity of Nek2 and seems constitutive. On progression from pachytene to metaphase, Nek2 is activated and HMGA2 is phosphorylated in an MAPK-dependent manner. We also show that Nek2 phosphorylates in vitro HMGA2 and that this phosphorylation decreases the affinity of HMGA2 for DNA and might favor its release from the chromatin. Indeed, we find that most HMGA2 associates with chromatin in mouse pachytene spermatocytes, whereas it is excluded from the chromatin upon the G2/M progression. Because hmga2-/- mice are sterile and show a dramatic impairment of spermatogenesis, it is possible that the functional interaction between HMGA2 and Nek2 plays a crucial role in the correct process of chromatin condensation in meiosis.

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Caron, Leslie, Frédéric Bost, Matthieu Prot, Paul Hofman, and Bernard Binétruy. "A new role for the oncogenic high-mobility group A2 transcription factor in myogenesis of embryonic stem cells." Oncogene 24, no. 41 (June 20, 2005): 6281–91. http://dx.doi.org/10.1038/sj.onc.1208781.

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33

Miao, Yi, Tengjiao Cui, Fenfei Leng, and W. David Wilson. "Inhibition of high-mobility-group A2 protein binding to DNA by netropsin: A biosensor-surface plasmon resonance assay." Analytical Biochemistry 374, no. 1 (March 2008): 7–15. http://dx.doi.org/10.1016/j.ab.2007.10.023.

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34

Kalomoiris, Stefanos, Andrew C. Cicchetto, Kinga Lakatos, Jan A. Nolta, and Fernando A. Fierro. "Fibroblast Growth Factor 2 Regulates High Mobility Group A2 Expression in Human Bone Marrow-Derived Mesenchymal Stem Cells." Journal of Cellular Biochemistry 117, no. 9 (March 8, 2016): 2128–37. http://dx.doi.org/10.1002/jcb.25519.

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35

Copley, Michael R., David G. Kent, Claudia Benz, Keegan M. Rowe, Stefan H. Woehrer, and Connie J. Eaves. "Evidence That High-Mobility Group A2 (Hmga2) Expression Contributes to the Ontogeny-Dependent Properties of Fetal Hematopoietic Stem Cells." Blood 116, no. 21 (November 19, 2010): 2634. http://dx.doi.org/10.1182/blood.v116.21.2634.2634.

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Abstract Abstract 2634 Fetal and early neonatal hematopoietic stem cells (HSCs) are distinct from their adult counterparts by their rapid turnover and expansion rates in vivo. However, the mechanisms underlying the regulation of these properties are poorly understood. In previous studies using serial limiting-dilution competitive repopulating transplant assays, our lab has shown that the rapid expansion phenotype of fetal HSCs is at least partially intrinsically determined since significantly more daughter HSCs are produced from fetal as compared to adult HSCs when similar numbers are transplanted into the same type of irradiated adult host. Additionally, we have observed a conversion of fetal HSCs to the adult regeneration phenotype that occurs within six weeks of transplantation in the primary host. To facilitate a comparison of highly-purified subsets of fetal and adult HSCs identified by an identical phenotype, we adopted the use of the CD45+EPCR+CD150+CD48− (E-SLAM) phenotype which we found gave HSC purities of 20–50% for hematopoietic tissues from early fetal to aged adulthood. We then used comparative gene expression analysis to identify candidate regulators of the fetal HSC high self-renewal program. This gave 20 candidate genes whose transcript levels were measured by quantitative real time PCR in E-SLAM cells isolated from E14.5 fetal liver (FL) and adult bone marrow (ABM). Of these genes only Hmga2 and Smarcc1 showed significant differences (p<.05) in expression between fetal and adult HSCs and only Hmga2 maintained this differential expression when the same cells were stimulated to divide for 48 hrs in vitro. To test the hypothesis that high expression of Hmga2 is a necessary and sufficient factor in determining the fetal HSC self-renewal program, purified adult E-SLAM HSCs were transduced with Hmga2-overexpressing or control lentiviruses and the kinetics of transduced vs untransduced hematopoietic cells in a congenic serial-transplantation model were then analyzed. Interestingly, when BM cells from the primary repopulated mice (transplanted 6-weeks earlier) were injected into secondary animals and the peripheral blood was analyzed for donor-type %Y/GFP chimerism, the Hmga2-overexpressing cells were observed to have a competititve advantage and exhibited an ∼6-fold expansion relative to the untransduced cells. In contrast, the control virus-infected BM cells were found to be equally competitive. These findings support the hypothesis that high expression of Hmga2 may be a critical mediator of the high self-renewal phenotype of fetal HSCs. Disclosures: No relevant conflicts of interest to declare.

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Lin, H. Helen, Ye Xiong, Ye-Shih Ho, Beiyun Zhou, Ha-Van Nguyen, Hongtao Deng, Renee Lee, Yun Yen, Zea Borok, and David K. Ann. "Transcriptional regulation by targeted expression of architectural transcription factor high mobility group A2 in salivary glands of transgenic mice." European Journal of Oral Sciences 115, no. 1 (February 2007): 30–39. http://dx.doi.org/10.1111/j.1600-0722.2007.00421.x.

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Motoyama, Kazuo, Hiroshi Inoue, Yoshito Nakamura, Hiroyuki Uetake, Kenichi Sugihara, and Masaki Mori. "Clinical Significance of High Mobility Group A2 in Human Gastric Cancer and Its Relationship to let-7 MicroRNA Family." Clinical Cancer Research 14, no. 8 (April 15, 2008): 2334–40. http://dx.doi.org/10.1158/1078-0432.ccr-07-4667.

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38

El-Hennawi, Diaa El-Din, Mohamed El Tabbakh, Nagwan Sabek, Ashraf Abou-halawa, and Amr Fareed. "High Mobility Group A2 (HMGA2) and Matrix Metalloproteinase 12 (MMP12) Genes Expression in Egyptian Patients with Laryngeal Squamous Cell Carcinoma." Egyptian Journal of Ear, Nose, Throat and Allied Sciences 20, no. 2 (July 1, 2019): 94–98. http://dx.doi.org/10.21608/ejentas.2019.6403.1056.

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39

Campbell, Taaliah, Ohuod Hawsawi, Nathan Bowen, and Valerie Odero-Marah. "Abstract 113: Investigating the role of high mobility group a2 (HMGA2) truncated isoform in promoting oxidative stress in PCa cells." Cancer Research 82, no. 12_Supplement (June 15, 2022): 113. http://dx.doi.org/10.1158/1538-7445.am2022-113.

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Abstract Prostate cancer (PCa) is one of the most commonly diagnosed malignancies among men worldwide and remains the second leading cause of cancer related death in the United States. Oxidative stress has been shown to be increase in several cancers including prostate cancer. In fact, oxidative stress in prostate cancer is suggested to be a direct result of cell exposure to reactive oxygen species (ROS). High mobility group A 2 (HMGA2), a non-histone protein, is an oncogene that is up-regulated in several cancers. This protein has ability to undergo chromosomal rearrangement and alternative splicing, causing its full length/wild type HMGA2 (HMGA2-WT) to become the truncated losing its 3’UTR leading to the generation of HMGA2 truncated (HMGA2-TR). We have previously shown HMGA2-WT’s involvement in epithelial mesenchymal transition (EMT), however, the functional role of HMGA2-TR has not yet been dissected. We hypothesize that truncated HMGA2’s involvement with oxidative stress leads to prostate cancer progression. We analyzed the baseline expression of wild-type vs.truncated HMGA2 in prostate patient tissue and cells lines by real-time PCR and western blot analyses. Prostate cancer patient tissue and some cell lines expressed increasing amounts of both wild-type and truncated HMGA2with increasing tumor grade, when compared to normal epithelial cells. RNA-Seq analysis of LNCaP prostate cancer cells stably overexpressing HMGA2-WT, HMGA2-TR, or empty vector (Neo) control revealed thatHMGA2-TR cells display increased oxidative stress compared to HMGA2-WT or Neo control cells. This was also confirmed by analysis of basal reactive oxygen species (ROS) levels, and the ratio of GSH/GSSG andNADP/NADPH utilizing metabolomics. Additionally, proteomic analysis showed that HMGA2-TR protein interacted with several proteins, including a cytoplasmic stress granule protein G3BP1 that responds to oxidative stress. Transient knockdown of G3BP1 increased ROS in HMGA2-TR cells. These studies may therefore uncover novel role for truncated HMGA2 in oxidative stress. Acknowledgements: These studies were supported by the NIH/NIMHD/RCI Grant #5G12MD007590-31,NIH/NIGMS/RISE Grant #5R25GM060414 Citation Format: Taaliah Campbell, Ohuod Hawsawi, Nathan Bowen, Valerie Odero-Marah. Investigating the role of high mobility group a2 (HMGA2) truncated isoform in promoting oxidative stress in PCa cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 113.

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Tan, E.-Jean, Sylvie Thuault, Laia Caja, Tea Carletti, Carl-Henrik Heldin, and Aristidis Moustakas. "Regulation of Transcription Factor Twist Expression by the DNA Architectural Protein High Mobility Group A2 during Epithelial-to-Mesenchymal Transition." Journal of Biological Chemistry 287, no. 10 (January 11, 2012): 7134–45. http://dx.doi.org/10.1074/jbc.m111.291385.

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41

Rizzi, Claudio, Palmina Cataldi, Aldo Iop, Miriam Isola, Riccardo Sgarra, Guidalberto Manfioletti, and Vincenzo Giancotti. "The expression of the high-mobility group A2 protein in colorectal cancer and surrounding fibroblasts is linked to tumor invasiveness." Human Pathology 44, no. 1 (January 2013): 122–32. http://dx.doi.org/10.1016/j.humpath.2012.05.001.

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42

Cui, Lihong, Rongna Wei, Zhiqun Shang, and Jing Leng. "Increased expression of high-mobility group A2: A novel independent indicator of poor prognosis in patients with esophageal squamous cell carcinoma." Journal of Cancer Research and Therapeutics 12, no. 4 (2016): 1291. http://dx.doi.org/10.4103/0973-1482.180616.

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43

Wu, Haijun, Yu Liang, Lin Shen, and Liangfang Shen. "MicroRNA-204 modulates colorectal cancer cell sensitivity in response to 5-fluorouracil-based treatment by targeting high mobility group protein A2." Biology Open 5, no. 5 (April 19, 2016): 563–70. http://dx.doi.org/10.1242/bio.015008.

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44

DiMaio, Christopher J., Frances Weis-Garcia, Emilia Bagiella, Michelle K. Kim, Laura H. Tang, and Peter J. Allen. "Tu1217 Pancreatic Cyst Fluid Concentration of High-Mobility Group A2 (HMGA2) Protein Acts As a Differential Biomarker of Dysplasia in IPMN." Gastroenterology 144, no. 5 (May 2013): S—794—S—795. http://dx.doi.org/10.1016/s0016-5085(13)62933-9.

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Franco, R., F. Esposito, M. Fedele, G. Liguori, GM Pierantoni, G. Botti, D. Tramontano, A. Fusco, and P. Chieffi. "Detection of high-mobility group proteins A1 and A2 represents a valid diagnostic marker in post-pubertal testicular germ cell tumours." Journal of Pathology 214, no. 1 (2007): 58–64. http://dx.doi.org/10.1002/path.2249.

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Mohammadi, Ali, Behzad Mansoori, Pouria Savadi, Vahid khaze, Mahsa Minouei, Nigel A. J. McMillan, Somayeh Hallaj‐Nezhadi, and Behzad Baradaran. "Targeting of high mobility group A2 by small interfering RNA‐loaded nanoliposome‐induced apoptosis and migration inhibition in gastrointestinal cancer cells." Journal of Cellular Biochemistry 120, no. 6 (December 2, 2018): 9203–12. http://dx.doi.org/10.1002/jcb.28196.

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Romine, Lorene E., Jennifer R. Wood, LuAnne A. Lamia, Paul Prendergast, Dean P. Edwards, and Ann M. Nardulli. "The High Mobility Group Protein 1 Enhances Binding of the Estrogen Receptor DNA Binding Domain to the Estrogen Response Element." Molecular Endocrinology 12, no. 5 (May 1, 1998): 664–74. http://dx.doi.org/10.1210/mend.12.5.0111.

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Abstract We have examined the ability of the high-mobility group protein 1 (HMG1) to alter binding of the estrogen receptor DNA-binding domain (DBD) to the estrogen response element (ERE). HMG1 dramatically enhanced binding of purified, bacterially expressed DBD to the consensus vitellogenin A2 ERE in a dose-dependent manner. The ability of HMG1 to stabilize the DBD-ERE complex resulted in part from a decrease in the dissociation rate of the DBD from the ERE. Antibody supershift experiments demonstrated that HMG1 was also capable of forming a ternary complex with the ERE-bound DBD in the presence of HMG1-specific antibody. HMG1 did not substantially affect DBD-ERE contacts as assessed by methylation interference assays, nor did it alter the ability of the DBD to induce distortion in ERE-containing DNA fragments. Because HMG1 dramatically enhanced estrogen receptor DBD binding to the ERE, and the DBD is the most highly conserved region among the nuclear receptor superfamily members, HMG1 may function to enhance binding of other nuclear receptors to their respective response elements and act in concert with coactivator proteins to regulate expression of hormone-responsive genes.

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DiMaio, Christopher J., Frances Weis-Garcia, Emilia Bagiella, Laura H. Tang, and Peter J. Allen. "Pancreatic cyst fluid concentration of high-mobility group A2 protein acts as a differential biomarker of dysplasia in intraductal papillary mucinous neoplasm." Gastrointestinal Endoscopy 83, no. 6 (June 2016): 1205–9. http://dx.doi.org/10.1016/j.gie.2015.09.020.

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49

Pierantoni, Giovanna Maria, Palma Finelli, Emanuele Valtorta, Daniela Giardino, Ornella Rodeschini, Francesco Esposito, Marco Losa, Alfredo Fusco, and Lidia Larizza. "High-mobility group A2 gene expression is frequently induced in non-functioning pituitary adenomas (NFPAs), even in the absence of chromosome 12 polysomy." Endocrine-Related Cancer 12, no. 4 (December 2005): 867–74. http://dx.doi.org/10.1677/erc.1.01049.

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The high-mobility group A2 (HMGA2) gene has a critical role in benign tumors where it is frequently rearranged, and in malignant tumors, where it is overexpressed in the absence of structural modification of the HMGA2 locus. By previous fluorescence in situ hybridization (FISH) and reverse transcriptase PCR analyses on human prolactin-secreting pituitary adenomas we detected rearrangement of the HMGA2 gene and amplification of its native region associated with activated expression. These data indicated a role for the HMGA2 gene in the development of human pituitary prolactinomas, since they are consistent with the appearance of prolactin/growth hormone adenomas in transgenic mice overexpressing the HMGA2 gene. To assess a more general role for HMGA2 in pituitary oncogenesis, we investigated HMGA2 amplification and expression in a panel of non-functioning pituitary adenomas (NFPAs) which account for 25% of all pituitary adenomas. We provide evidence that out of 18 NFPA tumors tested, 12 expressed HMGA2, but, different from prolactinomas, only in two cases the upregulation of the gene could be associated with amplification and/or rearrangement of the HMGA2 locus. Increased dosage of chromosome 12 was found in the expressing and non-expressing NFPAs, confirming that this sole event is insufficient to drive up activation of the HMGA2 gene. A role for chromosome 12 polysomy to promote structural instability of HMGA2 is confirmed, but the mechanism via trisomy is less prevalent in the frequently diploid NFPAs than in the usually hyperdiploid prolactinomas. Micro-rearrangements of HMGA2 gene not detectable by FISH analysis and/or sequence alterations could contribute to upregulation of HMGA2 gene in pituitary adenomas of the NFPA subtype. However, it cannot be excluded that the HMGA2 overexpression may be due, in some NFPA patients, to the same, still mainly unknown, mechanisms responsible for HMGA2 overexpression in malignant neoplasias.

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Borrmann, L. "High mobility group A2 protein and its derivatives bind a specific region of the promoter of DNA repair gene ERCC1 and modulate its activity." Nucleic Acids Research 31, no. 23 (December 1, 2003): 6841–51. http://dx.doi.org/10.1093/nar/gkg884.

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