ArticleCancer management and research2019
OCT4 accelerates tumorigenesis through activating JAK/STAT signaling in ovarian cancer side population cells.
Article in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 53 citations in OpenAlex.
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- Effects of Thyroid Hormones on Cellular Development in Human Ovarian Granulosa Tumor Cells (KGN).Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Modulating the JAK/STAT pathway with natural products: potential and challenges in cancer therapy.Discover oncology · 2025Review
- Targeting TYK2 for Fighting Diseases: Recent Advance of TYK2 Inhibitors.Current medicinal chemistry · 2024Review
- Exploring the dynamic interplay between cancer stem cells and the tumor microenvironment: implications for novel therapeutic strategies.Journal of translational medicine · 2023Review
- Cancer Stem Cell Markers-Clinical Relevance and Prognostic Value in High-Grade Serous Ovarian Cancer (HGSOC) Based on The Cancer Genome Atlas Analysis.International journal of molecular sciences · 2023Article
- Endometrial and placental stem cells in successful and pathological pregnancies.Journal of assisted reproduction and genetics · 2023Review
- Deciphering Common Traits of Breast and Ovarian Cancer Stem Cells and Possible Therapeutic Approaches.International journal of molecular sciences · 2023Review
- Review
- Review
- Expression ofFrontiers in oncology · 2023Article
- "DEPHENCE" system-a novel regimen of therapy that is urgently needed in the high-grade serous ovarian cancer-a focus on anti-cancer stem cell and anti-tumor microenvironment targeted therapies.Frontiers in oncology · 2023Review
- Potential applications of JAK inhibitors, clinically approved drugs against autoimmune diseases, in cancer therapy.Frontiers in pharmacology · 2023Review
- JAK/STAT pathway: Extracellular signals, diseases, immunity, and therapeutic regimens.Frontiers in bioengineering and biotechnology · 2023Review
- Review
- In-depth analysis of the expression and functions of signal transducers and activators of transcription in human ovarian cancer.Frontiers in oncology · 2022Article
- IFN-γ inhibits ovarian cancer progression via SOCS1/JAK/STAT signaling pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Article
- Requirement of transcription factor NME2 for the maintenance of the stemness of gastric cancer stem-like cells.Cell death & disease · 2021Article
- Review
- Article
Corrections and comments
- Retracted
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough surgery, chemotherapy, and radiotherapy eliminate clinically apparent ovarian tumor, the 5-year survival rate is no more than 45%. Cancer stem cells (CSCs) have been identified for precaution of tumor metastasis and recurrence in many kinds of cancers including ovarian cancer.
aimThis study aims to explore the function of OCT4, a CSC marker, in ovarian cancer progression and to investigate its underlying mechanism. MATERIALS AND
methodsBy Hoechst side population (SP) technique, CSC-like SP cells from human ovarian cancer SKOV3 and A2780 cells were isolated and used for this study. shRNA and lentivirus targeting human
resultsResults showed that OCT4 was upregulated in the SP of SKOV3 and A2780 cells when compared with the NSP cells. Downregulation of OCT4 inhibited SP cell viability, tumorigenesis, and reduced cell drug resistance and induced a G2/M phase arrest, while upregulation of OCT4 conferred NSP cell malignant features. Besides, OCT4 upregulation in NSP cells increased the phosphorylated levels of proteins in JAK and STAT families, especially in JAK1 and STAT6. Furthermore, the roles of apoptosis inhibition and viability, invasion, and tumorigenesis promotions induced by OCT4 in NSP cells were all abolished when adding peficitinib.
conclusionOur study demonstrated that OCT4 accelerated ovarian cancer progression through activating JAK/STAT signaling pathway.
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