<scp>KLF</scp>5 strengthens drug resistance of ovarian cancer stem‐like cells by regulating survivin expression

Dong, Zhihao; Liu, Yang; Lai, Dongmei

doi:10.1111/cpr.12043

Cited by 60 publications

(46 citation statements)

References 39 publications

(54 reference statements)

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“…Moreover, Klf5 is essential for oncogenesis and can strengthen drug resistance in CSCs [17–19]. Zfp42 belongs to Myc-centered regulatory network, which is active in various cancers [20].…”

Section: Discussionmentioning

confidence: 99%

MBD3 inhibits formation of liver cancer stem cells

Han

et al. 2016

Oncotarget

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Liver cancer cells can be reprogrammed into induced cancer stem cells (iCSCs) by exogenous expression of the reprogramming transcription factors Oct4, Sox2, Klf4 and c-Myc (OSKM). The nucleosome remodeling and deacetylase (NuRD) complex is essential for reprogramming somatic cells. In this study, we investigated the function of NuRD in the induction of liver CSCs. We showed that suppression of methyl-CpG binding domain protein 3 (MBD3), a core subunit of the NuRD repressor complex, together with OSKM transduction, induces conversion of liver cancer cells into stem-like cells. Expression of the transcription factor c-JUN is increased in MBD3-depleted iCSCs, and c-JUN activates endogenous pluripotent genes and regulates iCSC-related genes. These results indicate that MBD3/NuRD inhibits the induction of iCSCs, while c-JUN facilitates the generation of CSC-like properties. The iCSC reprogramming approach devised here provides a novel platform for dissection of the disordered signaling in liver CSCs. In addition, our results indicate that c-JUN may serve as a potential target for liver cancer therapy.

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Section: Discussionmentioning

confidence: 99%

MBD3 inhibits formation of liver cancer stem cells

Han

et al. 2016

Oncotarget

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“…IGF-I (insulin-like growth factor-I) activated survivin expression in prostate cancer cells [19,20]. KLF5 transcription factor displayed positive effect on survivin expression in leukemia cells [21], and in ovarian CSC (cancer stem cells) [22]. In chondrocytes, DEC1-mediated apoptosis protection was achieved through the activation of survivin expression.…”

Section: Positive Regulation Of Survivin Expresssionmentioning

confidence: 99%

Insights into the Regulation of Survivin Expression in Tumors

Vachtenheim¹,

Vlčková²

2016

Single Cell Biol

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Survivin, an anti-apoptotic protein was found to be expressed in tumors, whereas in normal tissues the expression of this protein was shown to be absent or extremely low. Survivin exhibits multifunctional activity in tumor cells. Survivin is the smallest member of the inhibitor of apoptosis protein family and was demonstrated to have key roles in regulating cell division and inhibiting apoptosis. The cancer protein survivin was shown to be associated with tumor cell progression, invasiveness, resistance to therapeutics and poor prognosis. Its level in tumors is associated with deregulation of several oncogenic pathways. In this review, a delineation of survivin expression and progress in understanding the survivin transcriptional regulation with the emphasis of augmented apoptosis in cancer and its link to the Hedgehog pathway and cancer stem cells is discussed.

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“…The exact cause of epithelial ovarian cancer has not yet been determined, although follicle-stimulating hormone (FSH) and luteinizing hormone (LH) are understood to be associated with ovarian malignancy (2). With apoptosis and apoptosis-linked genes demonstrating key roles in ovarian cancer tumorigenesis (3,4), it is important to note that FSH has been previously reported to inhibit apoptosis in ovarian cancer cells (5). However, little is currently understood regarding the association between LH and apoptosis in ovarian cancer, with further investigation required.…”

Section: Introductionmentioning

confidence: 99%

Luteinizing hormone inhibits cisplatin-induced apoptosis in human epithelial ovarian cancer cells

et al. 2016

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Abstract. The elevation of Luteinizing hormone (LH) is commonly observed in epithelial ovarian cancer. This correlation suggests a causal relationship between LH and ovarian cancer. LH has been reported to inhibit apoptosis in ovarian cancer cells. Programmed cell death gene 6 (PDCD6), also known as apoptosis-linked gene-2, is an apoptotic mediator that is required for apoptosis to numerous death stimuli. Therefore, the aim of the present study was to determine whether PDCD6 may be induced by LH in ovarian cancer, and whether LH may affect the apoptosis through PDCD6. Flow cytometry was used to detect the effects of cisplatin on the induction of apoptosis by LH. PDCD6 expression was monitored by quantitative polymerase chain reaction and western blotting. The signaling transduction pathways were also investigated by western blotting. The present study demonstrated that LH reduced cisplatin-induced apoptosis in ovarian OVCAR-3 and SKOV-3 cancer cells. The results indicated that PDCD6 expression was inhibited by LH. In addition, the inhibition of PDCD6, induced by LH, was mediated through the activation of the phosphatidylinositol 3-kinase/protein kinase B and p44/42 mitogen-activated protein kinase transduction signaling pathways. The present results suggest that LH affects the sensitivity of ovarian cancer cells to chemotherapy, primarily by signaling to inhibit apoptosis and to additionally suppress PDCD6.

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KLF5 strengthens drug resistance of ovarian cancer stem‐like cells by regulating survivin expression

Abstract: The KLF5-mediated signalling pathway is a potential target for elimination of ovarian CSCs.

Cited by 60 publications

References 39 publications

MBD3 inhibits formation of liver cancer stem cells

MBD3 inhibits formation of liver cancer stem cells

Insights into the Regulation of Survivin Expression in Tumors

Luteinizing hormone inhibits cisplatin-induced apoptosis in human epithelial ovarian cancer cells

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