Relevant bibliographies by topics / Hepatocellular cancer, p21, p53

Academic literature on the topic 'Hepatocellular cancer, p21, p53'

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Published: 10 March 2023

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Journal articles on the topic "Hepatocellular cancer, p21, p53"

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Wang, Juan, Yuan Zhou, Chunyan Gu, Fang Ming, and Ying Zhang. "LncRNA SAMD12-AS1 Suppresses Proliferation and Migration of Hepatocellular Carcinoma via p53 Signaling Pathway." Journal of Oncology 2022 (August 23, 2022): 1–9. http://dx.doi.org/10.1155/2022/9096365.

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Purpose. Assessment of lncRNA SAMD12-AS1 expression in liver cancer tissues and cell lines to investigate the underlying molecular mechanisms that regulate liver cancer cell growth, development, invasion, and migration. Methods. The lncRNA SAMD12-AS1 expression in tumor tissues of 32 liver cancer patients was measured by real-time PCR, and its effect on the clinicopathological manifestations and liver cancer patients’ prognosis was determined. LncRNA SAMD12-AS1 overexpression and knockdown in liver cancer cell lines were established by cell transfection. The effects of lncRNA SAMD12-AS1 knockdown and overexpression on liver cancer cell growth, development, invasion, and migration were determined by MTT, Transwell, and clonogenic assays. Furthermore, its effects on the expression of E-cadherin, vimentin, p53, and p21 in hepatocellular carcinoma cells were determined by Western blot assay. Results. The level of lncRNA SAMD12-AS1 expression in tumor tissues was remarkably higher than that in paracancerous liver tissues ( p < 0.01 ). It was found that the lncRNA SAMD12-AS1 expression was largely correlated with TNM stage of tumor, vascular invasion, and hepatitis B surface (HBs) antigen in liver cancer patients ( p < 0.05 ). Cell function experiments showed that lncRNA SAMD12-AS1 overexpression promoted liver cancer development, migration, and invasion ( p < 0.05 ), while lncRNA SAMD12-AS1 knockdown inhibited the activity of liver cancer cells to invade and migrate ( p < 0.05 ). Western blot analysis showed that overexpression of lncRNA SAMD12-AS1 markedly inhibited p21, p53, and E-cadherin expression and promoted vimentin expression. Conversely, knockdown of lncRNA SAMD12-AS1 significantly promoted p21, p53, and E-cadherin expression and inhibited vimentin expression ( p < 0.05 ). Conclusion. LncRNA SAMD12-AS1 is associated with the TNM stage and vascular invasion of liver cancer. It promotes liver cancer cell development, invasion, and migration by regulating p53 expression. Thus, lncRNA SAMD12-AS1 could be a novel biological target for the treatment of liver cancer.
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Qin, Lan Fang, Irene O. L. Ng, Sheung T. Fan, and Matthew Ng. "p21/WAF1, p53 and PCNA expression andp53 mutation status in hepatocellular carcinoma." International Journal of Cancer 79, no. 4 (August 21, 1998): 424–28. http://dx.doi.org/10.1002/(sici)1097-0215(19980821)79:4<424::aid-ijc19>3.0.co;2-4.

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Zhang, Erlei, and Zhiyong Huang. "XRCC2 promotes cancer progression by regulating p53/p21 signaling pathway in hepatocellular carcinoma." HPB 21 (2019): S358—S359. http://dx.doi.org/10.1016/j.hpb.2019.10.1974.

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Zhang, E., Z. Huang, and X. Chen. "XRCC2 promotes cancer progression by regulating p53/p21 signaling pathway in hepatocellular carcinoma." HPB 20 (September 2018): S408—S409. http://dx.doi.org/10.1016/j.hpb.2018.06.2739.

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Huang, Jhen-Yu, You-Cian Lin, Han-Min Chen, Jiun-Tsai Lin, and Shao-Hsuan Kao. "Adenine Combined with Cisplatin Promotes Anticancer Activity against Hepatocellular Cancer Cells through AMPK-Mediated p53/p21 and p38 MAPK Cascades." Pharmaceuticals 15, no. 7 (June 26, 2022): 795. http://dx.doi.org/10.3390/ph15070795.

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Cisplatin has been widely used in cancer treatments. Recent evidence indicates that adenine has potential anticancer activities against various types of cancers. However, the effects of the combination of adenine and cisplatin on hepatocellular carcinoma (HCC) cells remain sketchy. Here, our objective was to elucidate the anticancer activity of adenine in combination with cisplatin in HCC cells and its mechanistic pathways. Cell viability and cell cycle progression were assessed by the SRB assay and flow cytometry, respectively. Apoptosis was demonstrated by PI/annexin V staining and flow cytometric analysis. Protein expression, signaling cascade, and mRNA expression were analyzed by Western blotting and quantitative RT-PCR, respectively. Our results showed that adenine jointly potentiated the inhibitory effects of cisplatin on the cell viability of SK-Hep1 and Huh7 cells. Further investigation showed that adenine combined with cisplatin induced higher S phase arrest and apoptosis in HCC cells. Mechanically, adenine induced AMPK activation, reduced mTOR phosphorylation, and increased p53 and p21 levels. The combination of adenine and cisplatin synergistically reduced Bcl-2 and increased PUMA, cleaved caspase-3, and PARP in HCC cells. Adenine also upregulated the mRNA expression of p53, p21, PUMA, and PARP, while knockdown of AMPK reduced the increased expression of these genes. Furthermore, adenine also induced the activation of p38 MAPK through AMPK signaling, and the inhibition of p38 MAPK reduced the apoptosis of HCC cells with exposure to adenine combined with cisplatin. Collectively, these findings reveal that the combination of adenine and cisplatin synergistically enhances apoptosis of HCC cells, which may be attributed to the AMPK-mediated p53/p21 and p38 MAPK cascades. It suggests that adenine may be a potential adjuvant for the treatment of HCC in combination with cisplatin.
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Wan, Xin-xing, Han-chun Chen, Md Asaduzzaman Khan, Ai-hua Xu, Fu-lan Yang, Yun-yi Zhang, and Dian-zheng Zhang. "ISG15 Inhibits IFN-α-Resistant Liver Cancer Cell Growth." BioMed Research International 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/570909.

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Hepatocellular carcinoma (HCC) is one of the most prevalent tumors worldwide. Interferon-α(IFN-α) has been widely used in the treatment of HCC, but patients eventually develop resistance. ISG15 ubiquitin-like modifier (ISG15) is a ubiquitin-like protein transcriptionally regulated by IFN-αwhich shows antivirus and antitumor activities. However, the exact role of ISG15 is unknown. In the present study, we showed that IFN-αsignificantly induced ISG15 expression but failed to induce HepG2 cell apoptosis, whereas transient overexpression of ISG15 dramatically increased HepG2 cell apoptosis. ISG15 overexpression increased overall protein ubiquitination, which was not observed in cells with IFN-α-induced ISG15 expression, suggesting that IFN-αtreatment not only induced the expression of ISG15 but also inhibited ISG15-mediated ubiquitination. The tumor suppressor p53 and p21 proteins are the key regulators of cell survival and death in response to stress signals such as DNA damage. We showed that p53 or p21 is only up regulated in HepG2 cells ectopically expressing ISG15, but not in the presence of IFN-α-induced ISG15. Our results suggest that ISG15 overexpression could be developed into a powerful gene-therapeutic tool for treating IFN-α-resistant HCC.
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Park, So Hyun, Ji-Young Hong, Hyen Joo Park, and Sang Kook Lee. "The Antiproliferative Activity of Oxypeucedanin via Induction of G2/M Phase Cell Cycle Arrest and p53-Dependent MDM2/p21 Expression in Human Hepatoma Cells." Molecules 25, no. 3 (January 23, 2020): 501. http://dx.doi.org/10.3390/molecules25030501.

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Oxypeucedanin (OPD), a furocoumarin compound from Angelica dahurica (Umbelliferae), exhibits potential antiproliferative activities in human cancer cells. However, the underlying molecular mechanisms of OPD as an anticancer agent in human hepatocellular cancer cells have not been fully elucidated. Therefore, the present study investigated the antiproliferative effect of OPD in SK-Hep-1 human hepatoma cells. OPD effectively inhibited the growth of SK-Hep-1 cells. Flow cytometric analysis revealed that OPD was able to induce G2/M phase cell cycle arrest in cells. The G2/M phase cell cycle arrest by OPD was associated with the downregulation of the checkpoint proteins cyclin B1, cyclin E, cdc2, and cdc25c, and the up-regulation of p-chk1 (Ser345) expression. The growth-inhibitory activity of OPD against hepatoma cells was found to be p53-dependent. The p53-expressing cells (SK-Hep-1 and HepG2) were sensitive, but p53-null cells (Hep3B) were insensitive to the antiproliferative activity of OPD. OPD also activated the expression of p53, and thus leading to the induction of MDM2 and p21, which indicates that the antiproliferative activity of OPD is in part correlated with the modulation of p53 in cancer cells. In addition, the combination of OPD with gemcitabine showed synergistic growth-inhibitory activity in SK-Hep-1 cells. These findings suggest that the anti-proliferative activity of OPD may be highly associated with the induction of G2/M phase cell cycle arrest and upregulation of the p53/MDM2/p21 axis in SK-HEP-1 hepatoma cells.
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Lin, Yi-Ting, Shu-Man Liang, Ya-Ju Wu, Yi-Ju Wu, Yi-Jhu Lu, Yee-Jee Jan, Bor-Sheng Ko, et al. "Cordycepin Suppresses Endothelial Cell Proliferation, Migration, Angiogenesis, and Tumor Growth by Regulating Focal Adhesion Kinase and p53." Cancers 11, no. 2 (February 1, 2019): 168. http://dx.doi.org/10.3390/cancers11020168.

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Focal adhesion kinase (FAK) plays an important role in vascular development, including the regulation of endothelial cell (EC) adhesion, migration, proliferation, and survival. 3’-deoxyadenosine (cordycepin) is known to suppress FAK expression, cell migration, and the epithelial–mesenchymal transition in hepatocellular carcinoma (HCC). However, whether cordycepin affects FAK expression and cellular functions in ECs and the specific molecular mechanism remain unclear. In this study, we found that cordycepin suppressed FAK expression and the phosphorylation of FAK (p-FAK) at Tyr397 in ECs. Cordycepin inhibited the proliferation, wound healing, transwell migration, and tube formation of ECs. Confocal microscopy revealed that cordycepin significantly reduced FAK expression and decreased focal adhesion number of ECs. The suppressed expression of FAK was accompanied by induced p53 and p21 expression in ECs. Finally, we demonstrated that cordycepin suppressed angiogenesis in an in vivo angiogenesis assay and reduced HCC tumor growth in a xenograft nude mice model. Our study indicated that cordycepin could attenuate cell proliferation and migration and may result in the impairment of the angiogenesis process and tumor growth via downregulation of FAK and induction of p53 and p21 in ECs. Therefore, cordycepin may be used as a potential adjuvant for cancer therapy.
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Abou-Alfa, G. K., R. D. Carvajal, K. Y. Chung, R. A. Ghossein, M. Capanu, M. Gonen, G. Jacobs, D. P. Kelsen, and G. K. Schwartz. "A non-randomized phase II study of sequential irinotecan (CPT) and flavopiridol (F) in patients (pts) with advanced hepatocellular carcinoma (HCC)." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 4148. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.4148.

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4148 Background: F is a CDK inhibitor which potentiates CPT- induced apoptosis. In a phase I trial of CPT 100mg/m2 followed 7 hours later by F given over 1 hour weekly for 4 out of 6 weeks (Shah, Clin Can Res 2005), 2 pts with advanced HCC had stable disease (SD) for 14+ months. In the same phase I study, patients who were p53 wild-type (negative p53 staining), and whose p21 remained stable or was non-detectable on the post-treatment biopsy, were noted to have SD or a partial response. Methods: Pts with advanced HCC, no prior systemic therapy, Child’s-Pugh score A, B7 or B8, and KPS ≥ 70%, received 100 mg/m2 of CPT, followed 7 hours later by 60 mg/m2 of F over 1 hour weekly for 4 out of 6 weeks. The trial had a two stage design, with a planned accrual of 30 pts. The primary endpoint was TTP. Tumor response was assessed every 2 cycles using revised WHO criteria. p53 immuno-staining was performed on pre-treatment paraffin preserved tissues. A cut-off of 20% defined positive mutant versus negative wild-type p53 status. Results: 16 pts were enrolled: median age 64 (range 26–84), KPS 80% (70–90%), and 10 males/6 females. 13 pts received therapy, two progressed before starting, and one patient (pt) was excluded because pathology re-review did not confirm HCC. 1 pt was excluded because of consent withdrawal after first dose of therapy. This pt was included in the toxicity analysis. The median number of cycles given was 2 (range 1–8 cycles). Grade 3 and 4 toxicities included dehydration (4: 30%) diarrhea (2: 15%) febrile neutropenia (6: 46% - 4 events in one pt) and fatigue/weakness (3: 23%). Therapy had to be discontinued in 2 pts because of toxicity. TTP was 2.6 months (95% CI 2.43–8.42). One patient had SD for over a year, 8 had progression of disease (POD), and 4 came off study because of toxicity. Mutational p53 was evaluated in 7 pts. The pt with SD had wild type p53. Three pts with POD had mutant p53, while the other 3 had wild type 53. Conclusions: CPT followed by F is an ineffective therapy for HCC. This therapy was relatively poorly tolerated, likely contributed to by underlying cirrhosis in HCC, but similar to our experience of CPT in HCC. While p21 level pre and post therapy is lacking, the wild type p53 of the patient with SD maybe a predictor of response in HCC where p53 mutations are common. No significant financial relationships to disclose.
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Yang, Taewoo, Yegyun Choi, Jae Won Joh, Steve K. Cho, Dae-Shick Kim, and Sung-Gyoo Park. "Phosphorylation of p53 Serine 15 Is a Predictor of Survival for Patients with Hepatocellular Carcinoma." Canadian Journal of Gastroenterology and Hepatology 2019 (February 7, 2019): 1–8. http://dx.doi.org/10.1155/2019/9015453.

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Background. Hepatocellular carcinoma (HCC) is one of the most common malignant cancers with a poor prognosis. Several commonly investigated immunohistochemical markers in resected HCC have potential prognostic value, but the prognostic utility of p53 expression in HCC has remained elusive. Aim. To evaluate the prognostic value of p53 and p53 phosphorylation at serine 15 (p53 Ser15-P) in patients with HCC. Methods. Surgically resected tumors from 199 HCC patients were analyzed for p21, p53, p53 Ser15-P, and proliferating cell nuclear antigen (PCNA) expression using immunohistochemistry. Results. Stratifying by the expression of p53 Ser15-P (P = 0.016), but not by p53 (P = 0.301), revealed significantly different survival outcomes in patients with HCC. Moreover, our analysis demonstrated that patients who were PCNA-positive and p53 Ser15-P–negative had significantly worse survival outcomes (P = 0.001) than patients who were PCNA-positive and p53 Ser15-P–positive. Conclusions. P53 Ser15-P is associated with poor outcomes in patients with HCC, and this prognostic marker is useful for predicting the survival of patients with PCNA-positive HCC.
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Dissertations / Theses on the topic "Hepatocellular cancer, p21, p53"

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BENNETT, RICHARD A. "The p53-p21-Cyclin E Pathway in Centrosome Amplification and Chromosome Instability." University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1189188730.

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Lu, Wenjing, and 鲁文静. "The interaction of mortalin and p53 in human hepatocellular carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46330069.

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Lehmkuhl-Dakhwe, K. Virginia. "Regulation of p53, p21, ARF, BIM, and BAX by the Transcription Factor Trip-Br1." Ohio University / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1194549826.

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Enane, Francis Obunyakha. "HEPATOCYTE DIFFERENTIATION AND HEPATOCELLULAR CARCINOMA: RATIONALE FOR P53 INDEPENDENT THERAPY." Case Western Reserve University School of Graduate Studies / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=case1491570319727552.

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Campbell, Kevin. "The use of Sphingomyelin to protect against UV induced DNA damage in Human Keratinocytes." DigitalCommons@CalPoly, 2015. https://digitalcommons.calpoly.edu/theses/1413.

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Non melanoma skin cancer (NMSC) is a serious condition caused by chronic ultraviolet (UV) exposure that leads to DNA damage in skin. UV radiation has the potential to lead to DNA damage, which triggers biochemical pathways within a cell. The result is that the cell either undergoes cell cycle arrest, giving the cell time to repair DNA damage, or apoptosis. Sunscreen is the most commonly used treatment for preventing UV induced skin damage, but it involves a number of undesirable and toxic side effects including damaging the dermis, premature aging of skin and underweight child births. This has led to interest in finding safer alternatives to prevent UV damage without the negative side effects of sunscreen. In particular, bovine milk sphingomyelin (SM) is a compound that has the potential to protect against UV damage without any of the dangerous side effects of sunscreen. Here we present the use of SM for UV protection of human keratinocytes (KRTs) to prevent DNA mutations that result from UV exposure. In particular, analysis of the expression of DNA damage biomarkers p21 and p53 was done to determine the potential of SM to prevent DNA damage associated with UV exposure. Both non-SM treated KRTs and KRTs treated with 0.1% SM media 24 hours prior to UV radiation were fixed and IF-stained at 24 hours following 40 mJ/cm2 of UV exposure. Significant differences in both p21 and p53 were observed between the SM treated and non-SM treated cells at the UV dosage level (via t-test; p
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Sheel, Ankur. "Identification of Essential Genes in Hepatocellular Carcinomas using CRISPR Screening." eScholarship@UMMS, 2019. https://escholarship.umassmed.edu/gsbs_diss/1039.

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Hepatocellular carcinoma (HCC) is an aggressive subtype of liver cancer with a poor prognosis. Currently, prognosis for HCC patients remains poor as few therapies are available. The clinical need for more effective HCC treatments remains unmet partially because HCC is genetically heterogeneous and HCC driver genes amenable to targeted therapy are largely unknown. Mutations in the TP53 gene are found in ~30% of HCC patients and confer poor prognosis to patients. Identifying genes whose depletion can inhibit HCC growth, and determining the mechanisms involved, will aid the development of targeted therapies for HCC patients. Therefore, the first half of this thesis focuses on identifying genes that are required for cell growth in HCC independent of p53 status. We performed a kinome-wide CRISPR screen to identify genes required for cell growth in three HCC cell lines: HepG2 (p53 wild-type), Huh7 (p53-mutant) and Hep3B (p53-null) cells. The kinome screen identified 31 genes that were required for cell growth in 3 HCC cell lines independent of TP53 status. Among the 31 genes, 8 genes were highly expressed in HCC compared to normal tissue and increased expression was associated with poor survival in HCC patients. We focused on TRRAP, a co-factor for histone acetyltransferases. TRRAP function has not been previously characterized in HCC. CRISPR/Cas9 mediated depletion of TRRAP reduced cell growth and colony formation in all three cell lines. Moreover, depletion of TRRAP reduced its histone acetyltransferase co-factors KAT2A and KAT5 at the protein level with no change at the mRNA level. I found that depletion of KAT5, but not KAT2A, reduced cell growth. Notably, inhibition of proteasome- and lysosome-mediated degradation failed to rescue protein levels of KAT2A and KAT5 in the absence of TRRAP. Moreover, tumor initiation in an HCC mouse model failed after CRISPR/Cas9 depletion of TRRAP due to clearance via macrophages and HCC cells depleted of TRRAP and KAT5 failed to grow as subcutaneous xenografts in vivo. RNA-seq and bioinformatic analysis of HCC patient samples revealed that TRRAP positively regulates expression of genes that are involved in mitotic progression. In HCC, this subset of genes is clinically relevant as they are overexpressed compared to normal tissue and high expression confers poor survival to patients. I identified TOP2A as one of the mitotic gene targets of the TRRAP/KAT5 complex whose inhibition greatly reduces proliferation of HCC cells. Given that this was the first time the TRRAP/KAT5 complex has been identified as a therapeutic target in HCC, the second half of this thesis focuses on identifying the mechanism via which depletion of this complex inhibits proliferation of HCC cells. I discovered that depletion of TRRAP, KAT5 and TOP2A reduced proliferation of HCC cells by inducing senescence. Typically, senescence is an irreversible state of cell cycle arrest at G1 that is due to activation of p53/p21 expression, phosphorylation of RB, and DNA damage. Surprisingly, induction of senescence after loss of TRRAP, KAT5 and TOP2A arrested cells during G2/M and senescence was independent of p53, p21, RB and DNA damage. In summary, this thesis identifies TRRAP as a potential oncogene in HCC. I identified a network of genes regulated by TRRAP and its-cofactor KAT5 that promote mitotic progression. Moreover, I demonstrated that disruption of TRRAP/KAT5 and its downstream target gene TOP2A result in senescence of HCC cells independent of p53 status. Taken together, this work suggests that targeting the TRRAP/KAT5 complex and its network of target genes is a potential therapeutic strategy for HCC patients.
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Wilce, Alice J. "Understanding the function and mechanisms of intestinal cell kinase in the growth and survival of prostate cancer cells." Thesis, Queensland University of Technology, 2015. https://eprints.qut.edu.au/85439/1/Alice_Wilce_Thesis.pdf.

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This project was a step forward in discovering the potential role of intestinal cell kinase in prostate cancer development. Intestinal cell kinase was shown to be upregulated in prostate cancer cells and altered expression led to changes in key cell survival proteins. This study used in vitro experiments to monitor changes in cell growth, protein and RNA expression.
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Morrison, Chevaun Danielle. "DYNAMIC INTERACTIONS OF P53 AND C-ABL IN REGULATING BREASTCANCER PROGRESSION AND METASTASIS." Case Western Reserve University School of Graduate Studies / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=case1481208229508494.

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Roger, Lauréline. "Etude des mécanismes de la régulation de l'EMT par le suppresseur de tumeur p53 dans un modèle de cellules de carcinome du colon." Montpellier 2, 2007. http://www.theses.fr/2007MON20182.

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Le suppresseur de tumeur p53 est un facteur de transcription impliqué dans la progression du cycle cellulaire et dans l'apoptose. Outre ses fonctions majeures, p53 régule également la migration et l'adhérence cellulaire qui sont deux évènements impliqués dans le processus métastatique. L'évolution maligne d'un carcinome peut aussi impliquer la répression transcriptionnelle de CDH1, qui code pour la E-cadhérine, protéine constitutive des jonctions adhérentes. Nous avons recherché si et comment p53 régule certains évènements moléculaires qui contrôle le processus métastatique. Nous montrons que la forme sauvage de p53 réprime directement la transcription de CDH1 dans des lignées cellulaires humaines de carcinome du colon (HCT116). Cette répression est associée à une expression de novo de la vimentine et à l'acquisition d'une morphologie plus fibroblastique. L'une des cibles transcriptionnelle majeure de p53, p21WAF1 court-circuite l'effet répresseur de p53 sur la transcription de CDH1. Trois mutants dominant-négatifs de p53 (R273H, R175H et V143A) répriment également la transcription de CDH1. De plus, l'expression stable du mutant V143A dans les cellules HCT116 p53-/- mime partiellement le phénotype observé suite l'accumulation aberrante de p53. De façon surprenante, ce phénotype mésenchymateux n'est pas associé à une augmentation des propriétés invasives. Ce travail implique p53 dans la régulation d'évènements moléculaires qui peuvent conduire à l'acquisition d'un phénotype mésenchymateux
The p53 tumour suppressor gene encodes a transcriptional regulator that monitor proliferation signals to prevent cells from uncontrolled growth. However, p53 has also alternative functions. Notably, loss of p53 favours cell migration and invasion, processes involved in tumour metastasis. Given that epithelial to mesenchymal transition (EMT) also increases cell migration by altering the cell phenotype and morphology, we hypothesized that p53 controls molecular alterations that mediate EMT during cancer progression. Analysis of E-cadherin promoter activity and chromatin immunoprecipitation identified p53 as a direct transcriptional repressor of E-cadherin in human colon carcinoma cells, HCT116. Aberrant levels of p53 disrupted E-Cadherin-based cell-cell contacts and induced a more mesenchymal phenotype with downregulation of E-Cadherin and induction of the mesenchymal gene, vimentin. In addition, p21Waf-1 impeded p53 transcriptional repression and restored in part cell to cell adhesion. Furthermore, HCT116p53-/- cells overexpressing dominant-negative form of p53 also displayed the EMT-like phenotype. Neither p53 nor mutant p53–mediated shift toward mesenchymal morphology led to an increase of cell invasiveness. This work and our previous finding of mutant p53-mediated cell invasion identify p53 as a novel regulator of EMT and offer new perspectives in the comprehension of metastasis
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Harr, Michael. "The Interactive Transcript Abundance Index [c-myc*p73á]/[p21*Bcl-2] Correlates With Spontaneous Apoptosis and Response to CPT-11: Implications for Predicting Chemoresistance and Cytotoxicity to DNA Damaging Agents." University of Toledo Health Science Campus / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=mco1176730845.

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Book chapters on the topic "Hepatocellular cancer, p21, p53"

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Elledge, Richard M., and D. Craig Allred. "Prognostic and predictive value of p53 and p21 in breast cancer." In Prognostic variables in node-negative and node-positive breast cancer, 169–88. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5195-9_14.

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Jia, Libin, Xin Wei Wang, Zongtang Sun, and Curtis C. Harris. "Interactive Effects of p53 Tumor Suppressor Gene and Hepatitis B Virus in Hepatocellular Carcinogenesis." In Molecular Pathology of Gastroenterological Cancer, 209–18. Tokyo: Springer Japan, 1997. http://dx.doi.org/10.1007/978-4-431-65915-0_15.

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Mydlo, Jack H., and Paul Crispen. "Angiogenesis, Growth Factors, Microvessel Density, p53 and p21 in Prostate Cancer." In Prostate Cancer, 63–68. Elsevier, 2003. http://dx.doi.org/10.1016/b978-012286981-5/50009-4.

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Boussettine, Rihabe, Youssef Ennaji, Najwa Hassou, Hlima Bessi, and Moulay Mustapha Ennaji. "In vivo gene therapy with p53 or p21 adenovirus for prostate cancer." In Oncogenic Viruses, 387–415. Elsevier, 2023. http://dx.doi.org/10.1016/b978-0-12-824152-3.00010-x.

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Lu, Yuan, Sara K. Drenkhahn, Glenn A. Jackson, Nicholas JE Starkey, and Dennis B. Lubahn. "Regulation of the p53 Pathway by Human Estrogen-Related Receptor β in Prostate Cancer Cells." In BASIC - Regulation of Nuclear Receptors & Gene Expression, P2–15—P2–15. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.p21.p2-15.

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Conference papers on the topic "Hepatocellular cancer, p21, p53"

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Xu, Weiguo, and Dawei Li. "Abstract 269: A novel mechanism of p21 induction by oxaliplatin in p53 deficient cancer cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-269.

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Li, G., S. S. Nair, S. J. Lees, and F. W. Booth. "Regulation of G2/M Transition in Mammalian Cells by Oxidative Stress." In ASME 2005 International Mechanical Engineering Congress and Exposition. ASMEDC, 2005. http://dx.doi.org/10.1115/imece2005-82349.

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The regulation of the G2/M transition for the mammalian cell cycle has been modeled using 19 states to investigate the G2 checkpoint dynamics in response to oxidative stress. A detailed network model of G2/M regulation is presented and then a “core” subsystem is extracted from the full network. An existing model of Mitosis control is extended by adding two important pathways regulating G2/M transition in response to DNA damage induced by oxidative stress. Model predictions indicate that the p53 dependent pathway is not required for initial G2 arrest as the Chk1/Cdc25C pathway can arrest the cell in G2 right after DNA damage. However, p53 and p21 expression is important for a more sustained G2 arrest by inhibiting the Thr161 phosphorylation by CAK. By eliminating the phosphorylation effect of Chk1 on p53, two completely independent pathways are obtained and it is shown that it does not affect the G2 arrest much. So the p53/p21 pathway makes an important, independent contribution to G2 arrest in response to oxidative stress, and any defect in this pathway may lead to genomic instability and predisposition to cancer. Such strict control mechanisms probably provide protection for survival in the face of various environmental changes. The controversial issue related to the mechanism of inactivation of Cdc2 by p21 is addressed and simulation predictions indicate that G2 arrest would not be affected much by considering the direct binding of p21 to Cdc2/Cyclin B given that the inhibition of CAK by p21 is already present if the binding efficiency is within a certain range. Lastly, we show that the G2 arrest time in response to oxidative stress is sensitive to the p53 synthesis rate.
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Salleh, Mohd Nazil, Tan Mei Cheng, Thuaibah Hashim, Henkie Isahwan Ahamd Mulyadi Lai, and Wan Khairuzzaman Wan Ramli. "Abstract A51: p53 and p21 mRNA and protein expression in treated synthetic estrogen in mouse transgenic animal model." In Abstracts: Third AACR International Conference on Frontiers in Basic Cancer Research - September 18-22, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.fbcr13-a51.

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Ghannam, Dima, Eyal Jacob, Reli Kakun, Tanya Wasserman, Lina Korsensky, Ofir Sternfeld, Julia Kagan, et al. "Abstract GMM-045: PAX8 PLAYS AN ESSENTIAL ROLE IN HIGH GRADE SEROUS OVARIAN CANCER VIA ACTIVATION OF MUTANT P53 AND MISLOCALIZED P21." In Abstracts: 12th Biennial Ovarian Cancer Research Symposium; September 13-15, 2018; Seattle, Washington. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1557-3265.ovcasymp18-gmm-045.

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Wang, Wei, Xinyi Yang, Xu Zhang, Ming-hai Wang, Horrick Sharma, John K. Buolamwini, and Ruiwen Zhang. "Abstract 3834: JKA97, a novel anti-cancer candidate, induces G1 arrest via up-regulation of p21 in a p53-independent manner." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3834.

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Das, Viswanath, Narendran Annadurai, and Marián Hajdúch. "Abstract 4474: An intricate role of p53 and p21 in cellular alterations and drug penetration in spheroids of colorectal cancer cells." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4474.

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Keith, James, Somdutta Roy, and Martin Tenniswood. "Abstract B53: Post‐translational modification of p53 by HDAC inhibitors leads to selective assembly of transcriptional complexes at the p21 locus." In Abstracts: First AACR International Conference on Frontiers in Basic Cancer Research--Oct 8–11, 2009; Boston MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.fbcr09-b53.

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Kim, Eun Mi, and Hong-Duck Um. "Abstract 2307: The p53/p21 complex is a functional unit that regulates cancer cell invasion and apoptosis by targeting Bcl-2 family proteins." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2307.

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Jackson, James G., Leslie L. Chang, Alfonso Quintás-Cardama, Adel K. El-Naggar, and Guillermina Lozano. "Abstract 1235: Induction of a p21 mediated senescence program by p53 impairs the apoptotic response to chemotherapy and clinical outcome in breast cancer." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1235.

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Kovacevic, Zaklina, Sutharshani Sivagurunathan, Helena Mangs, Sherin Chikhani, and Des R. Richardson. "Abstract B172: The metastasis suppressor NDRG1 up‐regulates p21 in a p53‐independent manner in cancer cells: A novel insight into its antitumor function." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-b172.

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