ArticleMolecular cancer therapeutics2013
Bisphosphorylated PEA-15 sensitizes ovarian cancer cells to paclitaxel by impairing the microtubule-destabilizing effect of SCLIP.
Article in Molecular cancer therapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Beyond STMN1: stathmin-family control of microtubule dynamics and paclitaxel resistance in cancer.Frontiers in oncology · 2026Review
- Big data-based identification of methylated genes associated with drug resistance and prognosis in ovarian cancer.Medicine · 2020Article
- Article
- UNC-45A is preferentially expressed in epithelial cells and binds to and co-localizes with interphase MTs.Cancer biology & therapy · 2019Article
- Glycolysis inhibition via mTOR suppression is a key step in cardamonin-induced autophagy in SKOV3 cells.BMC complementary and alternative medicine · 2018Article
- Tuning microtubule dynamics to enhance cancer therapy by modulating FER-mediated CRMP2 phosphorylation.Nature communications · 2018Article
- Unique protein expression signatures of survival time in kidney renal clear cell carcinoma through a pan-cancer screening.BMC genomics · 2017Article
- Glutamine promotes ovarian cancer cell proliferation through the mTOR/S6 pathway.Endocrine-related cancer · 2015Article
- On the Quest of Cellular Functions of PEA-15 and the Therapeutic Opportunities.Pharmaceuticals (Basel, Switzerland) · 2015Review
- Development of PEA-15 using a potent non-viral vector for therapeutic application in breast cancer.Cancer letters · 2015Article
- Tissue Specific Promoters in Colorectal Cancer.Disease markers · 2015Review
- Phosphoprotein enriched in astrocytes (PEA)-15: a potential therapeutic target in multiple disease states.Pharmacology & therapeutics · 2014Review
- The roles of STMN3 in various cancers.Science progressReview
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Paclitaxel is a standard chemotherapeutic agent for ovarian cancer. PEA-15 (phosphoprotein enriched in astrocytes-15 kDa) regulates cell proliferation, autophagy, apoptosis, and glucose metabolism and also mediates AKT-dependent chemoresistance in breast cancer. The functions of PEA-15 are tightly regulated by its phosphorylation status at Ser104 and Ser116. However, the effect of PEA-15 phosphorylation status on chemosensitivity of cancer cells remains unknown. Here, we tested the hypothesis that PEA-15 phosphorylated at both Ser104 and Ser116 (pPEA-15) sensitizes ovarian cancer cells to paclitaxel. We first found that knockdown of PEA-15 in PEA-15-high expressing HEY and OVTOKO ovarian cancer cells resulted in paclitaxel resistance, whereas re-expression of PEA-15 in these cells led to paclitaxel sensitization. We next found that SKOV3.ip1-DD cells (expressing phosphomimetic PEA-15) were more sensitive to paclitaxel than SKOV3.ip1-AA cells (expressing nonphosphorylatable PEA-15). Compared with SKOV3.ip1-vector and SKOV3.ip1-AA cells, SKOV3.ip1-DD cells displayed reduced cell viability, inhibited anchorage-independent growth, and augmented apoptosis when treated with paclitaxel. Furthermore, HEY and OVTOKO cells displayed enhanced paclitaxel sensitivity when transiently overexpressing phosphomimetic PEA-15 and reduced paclitaxel sensitivity when transiently overexpressing nonphosphorylatable PEA-15. These results indicate that pPEA-15 sensitizes ovarian cancer cells to paclitaxel. cDNA microarray analysis suggested that SCLIP (SCG10-like protein), a microtubule-destabilizing protein, is involved in pPEA-15-mediated chemosensitization. We found that reduced expression and possibly posttranslational modification of SCLIP following paclitaxel treatment impaired the microtubule-destabilizing effect of SCLIP, thereby promoting induction of mitotic arrest and apoptosis by paclitaxel. Our findings highlight the importance of pPEA-15 as a promising target for improving the efficacy of paclitaxel-based therapy in ovarian cancer.
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