CD166 promotes the cancer stem-like properties of primary epithelial ovarian cancer cells

Kim, Dae Kyoung; Ham, Min Hee; Lee, Seo Yul; Shin, Min Joo; Kim, Ye Eun; Song, Parkyong; Suh, Dong Soo; Kim, Jae Ho

doi:10.5483/bmbrep.2020.53.12.102

Cited by 28 publications

(13 citation statements)

References 29 publications

(35 reference statements)

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“…OCT4 was reported to be remarkably high expressed in lung adenocarcinoma [19], colorectal cancer [20], cervical cancer [21], ovarian cancer [22], and so on. Our nding indicated that OCT4 could activate angiogenesis and promote ovarian cancer metastasis by regulating LRPPRC/ VEGFR2 axis.…”

Section: Discussionmentioning

confidence: 99%

OCT4 Promotes Ovarian Cancer Cell Metastasis and Angiogenesis via Modulating VEGFR2/LRPPRC Pathway

Xie

Wang

et al. 2021

Preprint

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Background: Due to its high ability of metastasis, ovarian cancer remains the most lethal gynecological malignancy, yet its underlying mechanism remains unconfirmed. Objectives: The main purpose is to probe into the role and regulation mechanism of octamer-binding transcription factor 4 (OCT4) in angiogenesis and metastasis in ovarian cancer.Methods: Immunohistochemistry (IHC) and immunofluorescence in epithelial ovarian cancer specimens and benign ovarian tumor samples were performed, followed by RNA-sequencing and examination of angiogenesis, cell migration and invasion in OCT4 knockdown cell lines and the controls. Co-Immunoprecipitation (Co-IP), mass spectrometry, immunoblotting, immunofluorescence and chromatin immunoprecipitation (ChIP) analyses were conducted along with models of zebrafishes and nude mice of transplanted tumors to gain insights into the specific functions and mechanisms of action of OCT4 in ovarian cancer.Results: Firstly, we discovered that OCT4 expression was enhanced in ovarian cancer tissues significantly, especially in the metastatic lesions, indicating that OCT4 might be a key for the metastasis of ovarian cancer. Furtherly, we observed and verified that OCT4 promoted cell migration and invasion, and induced angiogenesis in vitro and in vivo. Mechanistically, OCT4 modulated the transcription of leucine‑rich PPR motif‑containing protein (LRPPRC)，and furtherly interacted with vascular endothelial growth factor receptor 2 (VEGFR2)/LRPPRC complex and ultimately triggered the downstream FAK/AKT signaling pathway . Conclusions: Together, through models of ovarian cancer cells, zebrafishes and tumor-transplanted mice, this study highlighted the importance of OCT4/LRPPRC/VEGFR2 signaling axis in metastasis of ovarian cancer and angiogenesis. Thus, our finding supplied a potential novel molecular-targeted approach for the treatment of ovarian cancer.

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Section: Discussionmentioning

confidence: 99%

OCT4 Promotes Ovarian Cancer Cell Metastasis and Angiogenesis via Modulating VEGFR2/LRPPRC Pathway

Xie

Wang

et al. 2021

Preprint

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“…Tumorsphere volume area was measured using imagej [ 18 ]. The numbers of tumorspheres were counted under a microscope [ 21 ].…”

Section: Methodsmentioning

confidence: 99%

Autophagy inhibits cancer stemness in triple‐negative breast cancer via miR‐181a‐mediated regulation of ATG5 and/or ATG2B

et al. 2022

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Autophagy has a dual role in the maintenance of cancer stem cells (CSCs), but the precise relationship between autophagy and cancer stemness requires further investigation. In this study, it was found that luminal and triple‐negative breast cancers require distinct therapeutic approaches because of their different amounts of autophagy flux. We identified that autophagy flux was inhibited in triple‐negative breast cancer (TNBC) CSCs. Moreover, miRNA‐181a (miR‐181a) expression is upregulated in both TNBC CSCs and patient tissues. Autophagy‐related 5 (ATG5) and autophagy‐related 2B (ATG2B) participate in the early formation of autophagosomes and were revealed as targets of miR‐181a. Inhibition of miR‐181a expression led to attenuation of TNBC stemness and an increase in autophagy flux. Furthermore, treatment with curcumin led to attenuation of cancer stemness in TNBC CSCs; the expression of ATG5 and ATG2B was enhanced and there was an increase of autophagy flux. These results indicated that ATG5 and ATG2B are involved in the suppression of cancer stemness in TNBC. In summary, autophagy inhibits cancer stemness through the miR‐181a‐regulated mechanism in TNBC. Promoting tumor‐suppressive autophagy using curcumin may be a potential method for the treatment of TNBC.

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“…Our previous study showed that CD166 exhibits CSC-like properties in primary epithelial ovarian cancer cells. CD166 induced the expression of CSC markers such as OCT4, SOX2, and aldehyde dehydrogenase 1 A1 (ALDH1A1), and ABC transporters in both A2780-derived sphere-forming cells and primary ovarian CSCs, thus promoting CSC-like properties and chemoresistance [ 75 ]. A recent report indicated that CD133+/CD166+ cells are strongly stem-like cancer cells in human gastric adenocarcinoma, and that CD133+/CD166- cells exhibit self-renewal properties, colony formation capacity, and substantial migration activity [ 76 ].…”

Section: Cell Surface Markers Of Ovarian Cscsmentioning

confidence: 99%

Therapeutic Strategies for Targeting Ovarian Cancer Stem Cells

Yang

Kim

et al. 2021

IJMS

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Ovarian cancer is a fatal gynecological malignancy. Although first-line chemotherapy and surgical operation are effective treatments for ovarian cancer, its clinical management remains a challenge owing to intrinsic or acquired drug resistance and relapse at local or distal lesions. Cancer stem cells (CSCs) are a small subpopulation of cells inside tumor tissues, and they can self-renew and differentiate. CSCs are responsible for the cancer malignancy involved in relapses as well as resistance to chemotherapy and radiation. These malignant properties of CSCs are regulated by cell surface receptors and intracellular pluripotency-associated factors triggered by internal or external stimuli from the tumor microenvironment. The malignancy of CSCs can be attenuated by individual or combined restraining of cell surface receptors and intracellular pluripotency-associated factors. Therefore, targeted therapy against CSCs is a feasible therapeutic tool against ovarian cancer. In this paper, we review the prominent roles of cell surface receptors and intracellular pluripotency-associated factors in mediating the stemness and malignancy of ovarian CSCs.

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CD166 promotes the cancer stem-like properties of primary epithelial ovarian cancer cells

Cited by 28 publications

References 29 publications

OCT4 Promotes Ovarian Cancer Cell Metastasis and Angiogenesis via Modulating VEGFR2/LRPPRC Pathway

OCT4 Promotes Ovarian Cancer Cell Metastasis and Angiogenesis via Modulating VEGFR2/LRPPRC Pathway

Autophagy inhibits cancer stemness in triple‐negative breast cancer via miR‐181a‐mediated regulation of ATG5 and/or ATG2B

Therapeutic Strategies for Targeting Ovarian Cancer Stem Cells

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