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Artigos de revistas sobre o tema "Picropodophylline"

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Publicado: 22 de junho de 2024

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1

Roulland, Emmanuel, Emmanuel Bertounesque, Christiane Huel e Claude Monneret. "Synthesis of picropodophyllin homolactone". Tetrahedron Letters 41, n.º 35 (agosto de 2000): 6769–73. http://dx.doi.org/10.1016/s0040-4039(00)01136-9.

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2

Roulland, Emmanuel, Emmanuel Bertounesque, Christiane Huel e Claude Monneret. "ChemInform Abstract: Synthesis of Picropodophyllin Homolactone." ChemInform 31, n.º 45 (7 de novembro de 2000): no. http://dx.doi.org/10.1002/chin.200045231.

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3

Wen, Pu Hong. "Kinetic Investigation of Thermal Decomposition Reactions of Podophyllic Acid and Picropodophyllic Acid". Advanced Materials Research 391-392 (dezembro de 2011): 1230–34. http://dx.doi.org/10.4028/www.scientific.net/amr.391-392.1230.

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The thermal behavior and thermal decomposition kinetic parameters of podophyllic acid and picropodophyllic acid in a temperature-programmed mode have been investigated by means of DSC and TG-DTG. The kinetic model functions in differential and integral forms of the thermal decomposition reactions mentioned above for leading stage were established. The kinetic parameters of the apparent activation energy Ea and per-exponential factor A were obtained from analysis of the TG-DTG curves by integral and differential methods. The most probable kinetic model function of the decomposition reaction in differential form was 2/3•α-1/2 for podophyllic acid and 1/2• (1-α)-1 for picropodophyllic acid. The values of Ea indicated that the reactivity of picropodophyllic acid was highter than that of podophyllic acid in the thermal decomposition reaction. The values of the entropy of activation ΔS≠, enthalpy of activation ΔH≠ and free energy of activation ΔG≠ of the reactions were estimated.

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4

Guo, Hong Zhu, De An Guo, Xue Yan Fei, Ya Jun Cui e Jun Hua Zheng. "Biotransformation of Podophyllotoxin to Picropodophyllin by Microbes". Journal of Asian Natural Products Research 1, n.º 2 (dezembro de 1998): 99–102. http://dx.doi.org/10.1080/10286029808039850.

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5

Ohshima-Hosoyama, Sachiko, Tohru Hosoyama, Laura D. Nelon e Charles Keller. "IGF-1 receptor inhibition by picropodophyllin in medulloblastoma". Biochemical and Biophysical Research Communications 399, n.º 4 (setembro de 2010): 727–32. http://dx.doi.org/10.1016/j.bbrc.2010.08.009.

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6

Wu, Qi, Ai-Ling Tian, Guido Kroemer e Oliver Kepp. "Autophagy induction by IGF1R inhibition with picropodophyllin and linsitinib". Autophagy 17, n.º 8 (10 de junho de 2021): 2046–47. http://dx.doi.org/10.1080/15548627.2021.1936934.

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7

Berkowitz, David B., Sungjo Choi e Jun-Ho Maeng. "Enzyme-Assisted Asymmetric Total Synthesis of (−)-Podophyllotoxin and (−)-Picropodophyllin". Journal of Organic Chemistry 65, n.º 3 (fevereiro de 2000): 847–60. http://dx.doi.org/10.1021/jo991582+.

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8

Pohmakotr, Manat, Taweechote Komutkul, Patoomratana Tuchinda, Samrarn Prabpai, Palangpon Kongsaeree e Vichai Reutrakul. "Syntheses of (±)-thuriferic acid ethyl ester, its analogues and (±)-picropodophyllone". Tetrahedron 61, n.º 22 (maio de 2005): 5311–21. http://dx.doi.org/10.1016/j.tet.2005.03.069.

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9

Pullin, Robert D. C., Jonathan D. Sellars e Patrick G. Steel. "Silenes in organic synthesis: a concise synthesis of (±)-epi-picropodophyllin". Organic & Biomolecular Chemistry 5, n.º 19 (2007): 3201. http://dx.doi.org/10.1039/b710370k.

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10

Colón, Eugenia, Farasat Zaman, Magnus Axelson, Olle Larsson, Christine Carlsson-Skwirut, Konstantin V. Svechnikov e Olle Söder. "Insulin-Like Growth Factor-I Is an Important Antiapoptotic Factor for Rat Leydig Cells during Postnatal Development". Endocrinology 148, n.º 1 (1 de janeiro de 2007): 128–39. http://dx.doi.org/10.1210/en.2006-0835.

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The present investigation examines the influence of IGF-I and the role of IGF-I receptor (IGF-IR) in the apoptosis/survival of Leydig cells. Immunohistochemical analysis of the rat testis at different ages revealed that the level of the phosphorylated IGF-IR increases from birth to d 20 of postnatal life, remaining high in the adult testis. Western blotting revealed that this level is higher in Leydig cells isolated from 40-d-old than from 10- or 60-d-old rats. Application of the terminal deoxyribonucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling assay revealed that IGF-I decreases the level of apoptosis in Leydig cells at all stages of development, and the selective inhibitor of IGF-IR, picropodophyllin, blocks this antiapoptotic effect. The mechanism underlying the antiapoptotic action of IGF-I involves the phosphatidylinositol 3-kinase/Akt pathway, and in immature Leydig cells, this growth factor enhances the expression of Bcl-2 and cellular inhibitor of apoptosis proteins 2, while preventing activation of caspase-3 by cleavage. Furthermore, IGF-II and high concentrations of insulin also evoke phosphorylation of IGF-IR and, like IGF-I, enhance the expression of the steroidogenic acute regulatory protein by Leydig cells. Inhibition of IGF-IR by picropodophyllin decreases the survival of Leydig cells, both in the presence and absence of IGF-I, demonstrating that signaling via the IGF-IR plays an important role in Leydig cell survival.

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11

Zhao, Jing, Yajing Wang e Libiao Luan. "Star-Shaped Polycaprolactone-Polyethyleneglycol Copolymer Micelle-Like Nanoparticles for Picropodophyllin Delivery". Journal of Biomedical Nanotechnology 10, n.º 8 (1 de agosto de 2014): 1627–34. http://dx.doi.org/10.1166/jbn.2014.1835.

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12

Hashemi, Jamileh, Claire Worrall, Daiana Vasilcanu, Mårten Fryknäs, Luqman Sulaiman, Mohsen Karimi, Wen-Hui Weng et al. "Molecular Characterization of Acquired Tolerance of Tumor Cells to Picropodophyllin (PPP)". PLoS ONE 6, n.º 3 (14 de março de 2011): e14757. http://dx.doi.org/10.1371/journal.pone.0014757.

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13

Lu, Xiaosheng, Ledan Wang, Jie Mei, Xin Wang, Xueqiong Zhu, Qiong Zhang e Jieqiang Lv. "Picropodophyllin inhibits epithelial ovarian cancer cells in vitro and in vivo". Biochemical and Biophysical Research Communications 435, n.º 3 (junho de 2013): 385–90. http://dx.doi.org/10.1016/j.bbrc.2013.04.097.

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14

Berkowitz, David B., Sungjo Choi e Jun-Ho Maeng. "ChemInform Abstract: Enzyme-Assisted Asymmetric Total Synthesis of (-)-Podophyllotoxin and (-)-Picropodophyllin." ChemInform 31, n.º 23 (8 de junho de 2010): no. http://dx.doi.org/10.1002/chin.200023243.

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15

FENG, XIAOYING, EIMAN ALEEM, YINGBO LIN, MAGNUS AXELSON, OLLE LARSSON e THOMAS STRÖMBERG. "Multiple antitumor effects of picropodophyllin in colon carcinoma cell lines: Clinical implications". International Journal of Oncology 40, n.º 4 (6 de dezembro de 2011): 1251–58. http://dx.doi.org/10.3892/ijo.2011.1281.

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16

Wu, Xuping, Linda Sooman, Malin Wickström, Mårten Fryknäs, Christine Dyrager, Johan Lennartsson e Joachim Gullbo. "Alternative Cytotoxic Effects of the Postulated IGF-IR Inhibitor Picropodophyllin In Vitro". Molecular Cancer Therapeutics 12, n.º 8 (22 de maio de 2013): 1526–36. http://dx.doi.org/10.1158/1535-7163.mct-13-0091.

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17

Yin, Shu-Cheng, Wei Guo e Ze-Zhang Tao. "Picropodophyllin inhibits tumor growth of human nasopharyngeal carcinoma in a mouse model". Biochemical and Biophysical Research Communications 439, n.º 1 (setembro de 2013): 1–5. http://dx.doi.org/10.1016/j.bbrc.2013.08.050.

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18

Vitale, Maxime, Guillaume Prestat, David Lopes, David Madec, Claire Kammerer, Giovanni Poli e Leonard Girnita. "New Picropodophyllin Analogs via Palladium-Catalyzed Allylic Alkylation−Hiyama Cross-Coupling Sequences". Journal of Organic Chemistry 73, n.º 15 (agosto de 2008): 5795–805. http://dx.doi.org/10.1021/jo800707q.

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19

Ogiku, Tsuyoshi, Shin-ichi Yoshida, Tooru Kuroda, Masami Takahashi, Hiroshi Ohmizu e Tameo Iwasaki. "Syntheses of Aryltetralin Lignans: Concise Syntheses of (±)-Isopodophyllotoxone, (±)-Picropodophyllone and Their Related Compounds". Bulletin of the Chemical Society of Japan 65, n.º 12 (dezembro de 1992): 3495–97. http://dx.doi.org/10.1246/bcsj.65.3495.

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20

TOMIZAWA, MINORU, FUMINOBU SHINOZAKI, YASUFUMI MOTOYOSHI, TAKAO SUGIYAMA, SHIGENORI YAMAMOTO e MAKOTO SUEISHI. "Picropodophyllin and sorafenib synergistically suppress the proliferation and motility of hepatocellular carcinoma cells". Oncology Letters 8, n.º 5 (27 de agosto de 2014): 2023–26. http://dx.doi.org/10.3892/ol.2014.2484.

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21

OGIKU, T., S. YOSHIDA, T. KURODA, M. TAKAHASHI, H. OHMIZU e T. IWASAKI. "ChemInform Abstract: Syntheses of Aryltetralin Lignans: Concise Syntheses of (.+-.)- Isopodophyllotoxone, (.+-.)-Picropodophyllone and Related Compounds." ChemInform 24, n.º 15 (20 de agosto de 2010): no. http://dx.doi.org/10.1002/chin.199315280.

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22

Wong Te Fong, Anne-Christine, Thomas R. Eykyn, Harry G. Parkes, Aleksandra Bielen, Chris Jones, Ian R. Judson, John R. Griffiths, Martin O. Leach e Yuen-Li Chung. "Abstract B61: Picropodophyllin (PPP) increases glucose metabolism and lactate production in paediatric glioblastoma cells". Clinical Cancer Research 18, n.º 10 Supplement (15 de maio de 2012): B61. http://dx.doi.org/10.1158/1078-0432.mechres-b61.

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23

Meresse, Philippe, Claude Monneret e Emmanuel Bertounesque. "Synthesis of podophyllotoxin analogues: δ-lactone-containing picropodophyllin, podophyllotoxin and 4′-demethyl-epipodophyllotoxin derivatives". Tetrahedron 60, n.º 11 (março de 2004): 2657–71. http://dx.doi.org/10.1016/j.tet.2004.01.017.

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24

Lemaire, Miguel, Charlotte Fristedt, Prasoon Agarwal, Eline Menu, Els Van Valckenborgh, Elke De Bruyne, Anders Österborg et al. "The HDAC Inhibitor LBH589 Enhances the Antimyeloma Effects of the IGF-1RTK Inhibitor Picropodophyllin". Clinical Cancer Research 18, n.º 8 (5 de março de 2012): 2230–39. http://dx.doi.org/10.1158/1078-0432.ccr-11-1764.

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25

Zhang, Qi, Jing Pan, Ronald A. Lubet, Yian Wang e Ming You. "Targeting the insulin-like growth factor-1 receptor by picropodophyllin for lung cancer chemoprevention". Molecular Carcinogenesis 54, S1 (27 de agosto de 2014): E129—E137. http://dx.doi.org/10.1002/mc.22206.

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26

Bieghs, Liesbeth, Susanne Lub, Karel Fostier, Ken Maes, Els Van Valckenborgh, Eline Menu, Hans E. Johnsen et al. "The IGF-1 receptor inhibitor picropodophyllin potentiates the anti-myeloma activity of a BH3-mimetic". Oncotarget 5, n.º 22 (30 de abril de 2014): 11193–208. http://dx.doi.org/10.18632/oncotarget.1933.

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27

Dong, Lin, Meirong Du e Qianzhou Lv. "Picropodophyllin inhibits type I endometrial cancer cell proliferation via disruption of the PI3K/Akt pathway". Acta Biochimica et Biophysica Sinica 51, n.º 7 (6 de junho de 2019): 753–60. http://dx.doi.org/10.1093/abbs/gmz055.

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Abstract The type-I insulin-like growth factor receptor (IGF-IR) is overexpressed in endometrial cancer. High IGF-IR expression was considered as an important prognostic factor for tumor progression. The purpose of this study was to investigate the role and molecular mechanism of IGF-IR inhibitor picropodophyllin (PPP) in the growth and development of endometrial cancer. High expression of IGF-IR was observed in endometrial cancer tissues, as well as in ECC-1 and KLE cell lines. PPP suppressed the number of clones of ECC-1 and KLE cell lines; however, it had no significant effect on HEC-1-A cell line, which expressed lower IGF-IR than ECC-1 and KLE cell lines. Furthermore, PPP reduced cell proliferation capacity, inhibited the IGF-IR mRNA expression, and suppressed protein phosphorylation of IGF-IR and Akt in the three cell lines. In addition, PPP inhibited the protein expression of survivin in KLE cell line after 1 h of exposure, though this effect did not last for prolonged time. In conclusion, IGF-IR was mostly overexpressed in type I endometrial cancer. High IGF-IR expression was an important prognostic factor of tumor progression. PPP mediated the down-regulation of IGF-IR phosphorylation and inhibited cell proliferation via the PI3K/Akt signal pathway. PPP may have the potential to become a clinical treatment target in endometrial carcinoma.

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28

Yoshida, Shin-ichi, Takeshi Yamanaka, Tutomu Miyake, Yasunori Moritani, Hiroshi Ohmizu e Tameo Iwasaki. "Asymmetric syntheses of lignans utilizing novel diastereoselective Michael addition of cyanohydrin: Syntheses of (+)-fargesin and (−)-picropodophyllone". Tetrahedron 53, n.º 28 (julho de 1997): 9585–98. http://dx.doi.org/10.1016/s0040-4020(97)00643-1.

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29

Yin, S., A. Girnita, T. Stromberg, Z. Khan, S. Andersson, H. Zheng, C. Ericsson et al. "Targeting the insulin-like growth factor-1 receptor by picropodophyllin as a treatment option for glioblastoma". Neuro-Oncology 12, n.º 1 (20 de outubro de 2009): 19–27. http://dx.doi.org/10.1093/neuonc/nop008.

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30

YOSHIDA, S., T. YAMANAKA, T. MIYAKE, Y. MORITANI, H. OHMIZU e T. IWASAKI. "ChemInform Abstract: Asymmetric Syntheses of Lignans Utilizing Novel Diastereoselective Michael Addition of Cyanohydrin: Syntheses of (+)-Fargesin and (-)- Picropodophyllone." ChemInform 28, n.º 50 (2 de agosto de 2010): no. http://dx.doi.org/10.1002/chin.199750276.

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31

Waraky, Ahmed, Karen Akopyan, Vendela Parrow, Thomas Strömberg, Magnus Axelson, Lars Abrahmsén, Arne Lindqvist, Olle Larsson e Eiman Aleem. "Picropodophyllin causes mitotic arrest and catastrophe by depolymerizing microtubules via Insulin-like growth factor-1 receptor-independent mechanism". Oncotarget 5, n.º 18 (31 de julho de 2014): 8379–92. http://dx.doi.org/10.18632/oncotarget.2292.

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32

Economou, Mario A., Sandra Andersson, Diana Vasilcanu, Charlotta All-Ericsson, Eline Menu, Ada Girnita, Leonard Girnita, Magnus Axelson, Stefan Seregard e Olle Larsson. "Oral Picropodophyllin (PPP) Is Well Tolerated In Vivo and Inhibits IGF-1R Expression and Growth of Uveal Melanoma". Investigative Opthalmology & Visual Science 49, n.º 6 (1 de junho de 2008): 2337. http://dx.doi.org/10.1167/iovs.07-0819.

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33

Economou, Mario A., Sandra Andersson, Diana Vasilcanu, Charlotta All-Ericsson, Eline Menu, Ada Girnita, Leonard Girnita, Magnus Axelson, Stefan Seregard e Olle Larsson. "Oral picropodophyllin (PPP) is well tolerated in vivo and inhibits IGF-1R expression and growth of uveal melanoma". Acta Ophthalmologica 86, esis4 (19 de novembro de 2008): 35–41. http://dx.doi.org/10.1111/j.1755-3768.2008.01184.x.

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34

Jiang, Li-hua, Nian-yun Yang, Xiao-lin Yuan, Yi-jie Zou, Ze-qun Jiang, Feng-ming Zhao, Jian-ping Chen, Ming-yan Wang e Da-xiang Lu. "Microarray Analysis of mRNA and MicroRNA Expression Profile Reveals the Role ofβ-Sitosterol-D-glucoside in the Proliferation of Neural Stem Cell". Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/360302.

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Neural stem cells (NSCs) are self-regenerating cells, but their regenerative capacity is limited. The present study was conducted to investigate the effect ofβ-sitosterol-D-glucoside (BSSG) on the proliferation of hippocampal NSCs and to determine the corresponding molecular mechanism. Results of CCK-8 assay showed that BSSG significantly increased NSC proliferation and the effectiveness of BSSG was similar to that of basic fibroblast growth factor and epidermal growth factor. mRNA expression profiling showed that 960 genes were differentially expressed after NSCs were treated with BSSG. Among the 960 genes, IGF1 is considered as a key regulatory gene that functionally promotes NSC proliferation. MicroRNA (miRNA) expression profiling indicated that 30 and 84 miRNAs were upregulated and downregulated, respectively. miRNA-mRNA relevance analysis revealed that numerous mRNAs including IGF1 mRNA were negatively regulated by miRNAs with decreased expression, thereby increasing the corresponding mRNA expression. The increased expression of IGF1 protein was validated by ELISA. Picropodophyllin (PPP, an inhibitor of IGF-1R) inhibition test confirmed that the proliferation-enhancing effect depended on IGF1. This study provided information about BSSG as an efficient and inexpensive growth factor alternative, of which the effect is closely involved in IGF1.

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35

Conti, Laura, Gabriella Regis, Angela Longo, Paola Bernabei, Roberto Chiarle, Mirella Giovarelli e Francesco Novelli. "In the absence of IGF-1 signaling, IFN-γ suppresses human malignant T-cell growth". Blood 109, n.º 6 (5 de dezembro de 2006): 2496–504. http://dx.doi.org/10.1182/blood-2006-07-034231.

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Abstract Several approaches to target insulin-like growth factor-1 (IGF-1) signaling have resulted in the inhibition of the growth of a broad range of tumor cells. Malignant T cells are insensitive to the antiproliferative effects of the interferon-γ (IFN-γ)/signal transducer and activator of transcription 1 (STAT1) pathway because of the IGF-1–dependent internalization of the IFN-γR2 signaling chain. Here we show that human malignant T cells are also resistant to the growth inhibitory effect of both the IGF-1 receptor–specific inhibitor picropodophyllin (PPP) and retrovirus-mediated gene transfer of a dominant negative IGF-1 receptor. However, blockade of IGF-1 receptor perturbs IFN-γR2 internalization and induces its cell surface accumulation in malignant T cells. This allows the reinstatement of the IFN-γ–induced STAT1 activation, a high expression of proapoptotic molecules, and the suppression of malignant T-cell growth both in vitro and in vivo in a severe combined immunodeficiency (SCID) mouse model. These data indicate that the inhibition of IGF-1 signaling combined with IFN-γ administration could be a promising approach to suppress the growth of neoplastic T cells resistant to each treatment on its own.

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36

Gong, Wan, Naidan Zhang, Gang Cheng, Quanlong Zhang, Yuqiong He, Yi Shen, Qi Zhang, Bo Zhu, Qiaoyan Zhang e Luping Qin. "Rehmannia glutinosa Libosch Extracts Prevent Bone Loss and Architectural Deterioration and Enhance Osteoblastic Bone Formation by Regulating the IGF-1/PI3K/mTOR Pathway in Streptozotocin-Induced Diabetic Rats". International Journal of Molecular Sciences 20, n.º 16 (15 de agosto de 2019): 3964. http://dx.doi.org/10.3390/ijms20163964.

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Rehmanniae Radix Praeparata (RR, named as Shudihuang in traditional Chinese medicine), the steamed roots of Rehmannia glutinosa Libosch (Scrophulariaceae), has been demonstrated to have anti-diabetic and anti-osteoporotic activities. This study aimed to explore the protective effect and underlying mechanism of RR on diabetes-induced bone loss. It was found that RR regulated the alkaline phosphatase activity and osteocalcin level, enhanced bone mineral density, and improved the bone microarchitecture in diabetic rats. The catalpol (CAT), acteoside (ACT), and echinacoside (ECH) from RR increased the proliferation and differentiation of osteoblastic MC3T3-E1 cells injured by high glucose and promoted the production of IGF-1 and expression of related proteins in BMP and IGF-1/PI3K/mammalian target of rapamycin complex 1 (mTOR) signaling pathways. The verifying tests of inhibitors of BMP pathway (noggin) and IGF-1/PI3K/mTOR pathway (picropodophyllin) and molecular docking of IGF-1R further indicated that CAT, ACT, and ECH extracted from RR enhanced bone formation by regulating IGF-1/PI3K/mTOR signaling pathways. These findings suggest that RR may prove to be a promising candidate drug for the prevention and treatment of diabetes-induced osteoporosis.

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WU, YONG-TAO, BAO-JUN WANG, SHENG-WU MIAO e JIAN-JUN GAO. "Picropodophyllin inhibits the growth of Ewing's sarcoma cells through the insulin-like growth factor-1 receptor/Akt signaling pathway". Molecular Medicine Reports 12, n.º 5 (28 de agosto de 2015): 7045–50. http://dx.doi.org/10.3892/mmr.2015.4266.

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38

Liao, Fenfang, Yongheng Chen, Qingqing Wu, Jiaqi Wen, Xiangjie Chen, Weizhang Wang, Dan Xu e Manyu Liu. "Selective elimination of CML stem/progenitor cells by picropodophyllin in vitro and in vivo is associated with p53 activation". Biochemical and Biophysical Research Communications 579 (novembro de 2021): 1–7. http://dx.doi.org/10.1016/j.bbrc.2021.09.029.

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39

Vasilcanu, R., D. Vasilcanu, L. Rosengren, N. Natalishvili, B. Sehat, S. Yin, A. Girnita, M. Axelson, L. Girnita e O. Larsson. "Picropodophyllin induces downregulation of the insulin-like growth factor 1 receptor: potential mechanistic involvement of Mdm2 and β-arrestin1". Oncogene 27, n.º 11 (10 de setembro de 2007): 1629–38. http://dx.doi.org/10.1038/sj.onc.1210797.

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40

Mo, Hai-Ying, Qi-Yao Wei, Qiu-Hua Zhong, Xiao-Yun Zhao, Dan Guo, Jin Han, Wachiraporn Noracharttiyapot et al. "Cytochrome P450 27C1 Level Dictates Lung Cancer Tumorigenicity and Sensitivity towards Multiple Anticancer Agents and Its Potential Interplay with the IGF-1R/Akt/p53 Signaling Pathway". International Journal of Molecular Sciences 23, n.º 14 (16 de julho de 2022): 7853. http://dx.doi.org/10.3390/ijms23147853.

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Cytochrome P450 enzymes (CYP450s) exert mighty catalytic actions in cellular metabolism and detoxication, which play pivotal roles in cell fate determination. Preliminary data shows differential expression levels of CYP27C1, one of the “orphan P450s” in human lung cancer cell lines. Here, we study the functions of CYP27C1 in lung cancer progression and drug endurance, and explore its potential to be a diagnostic and therapeutic target for lung cancer management. Quantitative real-time PCR and immunoblot assays were conducted to estimate the transcription and protein expression level of CYP27C1 in human lung cancer cell lines, which was relatively higher in A549 and H1975 cells, but was lower in H460 cells. Stable CYP27C1-knockdown A549 and H1975 cell lines were established, in which these cells showed enhancement in cell proliferation, colony formation, and migration. In addition, aberrant IGF-1R/Akt/p53 signal transduction was also detected in stable CYP27C1-knockdown human lung cancer cells, which exhibited greater tolerance towards the treatments of anticancer agents (including vinorelbine, picropodophyllin, pacritinib, and SKLB610). This work, for the first time, reveals that CYP27C1 impacts lung cancer cell development by participating in the regulation of the IGF-1R/Akt/p53 signaling pathway, and the level of CYP27C1 plays indispensable roles in dictating the cellular sensitivity towards multiple anticancer agents.

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41

Menu, Eline, Helena Jernberg-Wiklund, Thomas Stromberg, Hendrik De Raeve, Leonard Girnita, Olle Larsson, Magnus Axelson et al. "Inhibiting the IGF-1 receptor tyrosine kinase with the cyclolignan PPP: an in vitro and in vivo study in the 5T33MM mouse model". Blood 107, n.º 2 (15 de janeiro de 2006): 655–60. http://dx.doi.org/10.1182/blood-2005-01-0293.

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AbstractInsulin-like growth factor 1 (IGF-1) plays a pleiotropic role in multiple myeloma (MM), that is, in survival, proliferation, chemotaxis, and angiogenesis. Strategies targeting the IGF-1 receptor (IGF-1R) may therefore be important to develop efficient anti-MM agents. In this work we investigated the effect of an IGF-1R tyrosine kinase (IGF-1RTK) inhibitor (picropodophyllin or PPP) in the 5T33MM mouse model. In vitro data showed that PPP reduced IGF-1R autophosphorylation and downstream ERK activation, leading to inhibition of IGF-1–stimulated proliferation and vascular endothelial growth factor (VEGF) secretion of MM cells. In an in vivo study, PPP reduced the bone marrow tumor burden and serum paraprotein in 5T33MM mice by 77% and 90%, respectively, compared to vehicle-treated animals. Angiogenesis was assessed by quantifying the microvessel density on CD31-stained paraffin sections and this was reduced by 60% in the PPP-treated group. In a separate survival experiment, Kaplan-Meier analysis demonstrated a significant increase in survival in PPP-treated 5T33MM animals compared to the vehicle controls (28 versus 18 days). These data suggest that the IGF-1RTK inhibitor PPP possesses a marked antitumor activity and strongly points to the possibility of using IGF-1R inhibitors in the treatment of MM.

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Takata, Sho, Hiromi Sakata-Haga, Hiroki Shimada, Tsuyoshi Tsukada, Daisuke Sakai, Hiroki Shoji, Mitsuhiro Tomosugi et al. "LIF–IGF Axis Contributes to the Proliferation of Neural Progenitor Cells in Developing Rat Cerebrum". International Journal of Molecular Sciences 23, n.º 21 (30 de outubro de 2022): 13199. http://dx.doi.org/10.3390/ijms232113199.

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In rodent models, leukemia inhibitory factor (LIF) is involved in cerebral development via the placenta, and maternal immune activation is linked to psychiatric disorders in the child. However, whether LIF acts directly on neural progenitor cells (NPCs) remains unclear. This study performed DNA microarray analysis and quantitative RT-PCR on the fetal cerebrum after maternal intraperitoneal or fetal intracerebral ventricular injection of LIF at day 14.5 (E14.5) and determined that the expression of insulin-like growth factors (IGF)-1 and -2 was induced by LIF. Physiological IGF-1 and IGF-2 levels in fetal cerebrospinal fluid (CSF) increased from E15.5 to E17.5, following the physiological surge of LIF levels in CSF at E15.5. Immunostaining showed that IGF-1 was expressed in the cerebrum at E15.5 to E19.5 and IGF-2 at E15.5 to E17.5 and that IGF-1 receptor and insulin receptor were co-expressed in NPCs. Further, LIF treatment enhanced cultured NPC proliferation, which was reduced by picropodophyllin, an IGF-1 receptor inhibitor, even under LIF supplementation. Our findings suggest that IGF expression and release from the NPCs of the fetal cerebrum in fetal CSF is induced by LIF, thus supporting the involvement of the LIF–IGF axis in cerebral cortical development in an autocrine/paracrine manner.

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Razuvaev, Anton, Bimma Henderson, Leonard Girnita, Olle Larsson, Magnus Axelson, Ulf Hedin e Joy Roy. "The cyclolignan picropodophyllin attenuates intimal hyperplasia after rat carotid balloon injury by blocking insulin-like growth factor-1 receptor signaling". Journal of Vascular Surgery 46, n.º 1 (julho de 2007): 108–15. http://dx.doi.org/10.1016/j.jvs.2007.02.066.

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Wu, Qi, Ai-Ling Tian, Bei Li, Marion Leduc, Sabrina Forveille, Peter Hamley, Warren Galloway et al. "IGF1 receptor inhibition amplifies the effects of cancer drugs by autophagy and immune-dependent mechanisms−". Journal for ImmunoTherapy of Cancer 9, n.º 6 (junho de 2021): e002722. http://dx.doi.org/10.1136/jitc-2021-002722.

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BackgroundPharmacological autophagy enhancement constitutes a preclinically validated strategy for preventing or treating most major age-associated diseases. Driven by this consideration, we performed a high-content/high-throughput screen on 65 000 distinct compounds on a robotized fluorescence microscopy platform to identify novel autophagy inducers.ResultsHere, we report the discovery of picropodophyllin (PPP) as a potent inducer of autophagic flux that acts on-target, as an inhibitor of the tyrosine kinase activity of the insulin-like growth factor-1 receptor (IGF1R). Thus, PPP lost its autophagy-stimulatory activity in cells engineered to lack IGF1R or to express a constitutively active AKT serine/threonine kinase 1 (AKT1) mutant. When administered to cancer-bearing mice, PPP improved the therapeutic efficacy of chemoimmunotherapy with a combination of immunogenic cytotoxicants and programmed cell death 1 (PDCD1, better known as PD-1) blockade. These PPP effects were lost when tumors were rendered PPP-insensitive or autophagy-incompetent. In combination with chemotherapy, PPP enhanced the infiltration of tumors by cytotoxic T lymphocytes, while reducing regulatory T cells. In human triple-negative breast cancer patients, the activating phosphorylation of IGF1R correlated with inhibited autophagy, an unfavorable local immune profile, and poor prognosis.ConclusionAltogether, these results suggest that IGF1R may constitute a novel and druggable therapeutic target for the treatment of cancer in conjunction with chemoimmunotherapies.

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Economou, Mario A., Jiangmei Wu, Daiana Vasilcanu, Linda Rosengren, Charlotta All-Ericsson, Ingeborg van der Ploeg, Eline Menu et al. "Inhibition of VEGF Secretion and Experimental Choroidal Neovascularization by Picropodophyllin (PPP), an Inhibitor of the Insulin-like Growth Factor-1 Receptor". Investigative Opthalmology & Visual Science 49, n.º 6 (1 de junho de 2008): 2620. http://dx.doi.org/10.1167/iovs.07-0742.

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Economou, Mario A., Jiangmei Wu, Daiana Vasilcanu, Linda Rosengren, Charlotta All-Ericsson, Ingeborg Van Der Ploeg, Eline Menu et al. "Inhibition of VEGF secretion and experimental choroidal neovascularization by picropodophyllin (PPP), an inhibitor of the insulin-like growth factor-1 receptor". Acta Ophthalmologica 86, esis4 (19 de novembro de 2008): 42–49. http://dx.doi.org/10.1111/j.1755-3768.2008.01185.x.

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E, Changyong, Jing Li, Dan Shao, Dan Zhang, Yue Pan, Li Chen e Xuewen Zhang. "The Insulin-Like Growth Factor-I Receptor Inhibitor Picropodophyllin-Induced Selective Apoptosis of Hepatocellular Carcinoma Cell Through a Caspase-Dependent Mitochondrial Pathway". Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 21, n.º 2 (10 de janeiro de 2014): 103–10. http://dx.doi.org/10.3727/096504013x13808175127324.

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Girnita, Ada, Charlotta All-Ericsson, Mario A. Economou, Kristina Astr√∂m, Magnus Axelson, Stefan Seregard, Olle Larsson e Leonard Girnita. "The insulin-like growth factor-I receptor inhibitor picropodophyllin causes tumor regression and attenuates mechanisms involved in invasion of uveal melanoma cells." Clinical Cancer Research 12, n.º 4 (15 de fevereiro de 2006): 1383–91. http://dx.doi.org/10.1158/1078-0432.ccr-05-1106.

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Duan, Zhenfeng, Edwin Choy, David Harmon, Cao Yang, Keinosuke Ryu, Joseph Schwab, Henry Mankin e Francis J. Hornicek. "Insulin-like growth factor-I receptor tyrosine kinase inhibitor cyclolignan picropodophyllin inhibits proliferation and induces apoptosis in multidrug resistant osteosarcoma cell lines". Molecular Cancer Therapeutics 8, n.º 8 (28 de julho de 2009): 2122–30. http://dx.doi.org/10.1158/1535-7163.mct-09-0115.

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Gullbo, Joachim, Michael Bergqvist, Malin Wickström, Peter Ericsson, Linda Sooman, Daniel Brattström, Stefan Bergström e Simon Ekman. "P3-016: In vitro activity of picropodophyllin in lung cancer cell lines and association to the insulin-like Growth Factor-1 receptor". Journal of Thoracic Oncology 2, n.º 8 (agosto de 2007): S613—S614. http://dx.doi.org/10.1097/01.jto.0000283773.72586.f8.

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