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BEX2 is poor prognostic factor and required for cancer stemness in gastric cancer [GCIY_siBEX2]

ABSTRACT: To investigate the BEX2 signaling, GCIY cells were knocked down using siRNA against BEX2.

ORGANISM(S): Homo sapiens

PROVIDER: GSE213836 | GEO | 2024/09/21

REPOSITORIES: GEO

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BEX2 is poor prognostic factor and required for cancer stemness in gastric cancer [MKN1_siBEX2]

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BEX2 is poor prognostic factor and required for cancer stemness in gastric cancer

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BEX2 is poor prognostic factor and required for cancer stemness in gastric cancer [GCIY_siBEX2]

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BEX2 is poor prognostic factor and required for cancer stemness in gastric cancer [MKN1_siBEX2]

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BEX2 is poor prognostic factor and required for cancer stemness in gastric cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

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BEX2 suppresses mitochondrial activity and is required for dormant cancer stem cell maintenance in intrahepatic cholangiocarcinoma

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Silencing of BEX2 promotes colorectal cancer metastasis through Hedgehog signaling pathway

Project description:Colorectal cancer is one of the most common cancers worldwide with increasing incidence, the presence of metastasis is one of the major causes for poor outcome. BEX2 has been reported to be involved in tumor development in several types of cancer, but is poorly understood in metastatic colorectal cancer. Here we demonstrated that knockout of BEX2 resulted in the enhancement of the migratory and metastatic potential of colorectal cancer cells in vivo and in vitro, re-expression of BEX2 in knockout cells could reverse the migratory enhancement. Expression profile chip indicated that hedgehog signaling pathway was activated after knockout of BEX2, and hedgehog Signaling inhibitor GANT61 and GDC-0449 could somehow reverse the migratory enhancement of BEX2-/- colorectal cancer cells. We also demonstrated that it is the nucleus translocation of Zic2 after BEX2 silenced, that activated hedgehog signaling pathway, while knockdown Zic2 could also abrogated migratory enhancement of BEX2-/- cells. In summary, our findings suggest that BEX2 is a negative modulator of hedgehog signaling pathway by retaining Zic2 in the cytoplasm of colorectal cancer cells, thus to inhibit colorectal cancer cell migration and metastasis.

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BEX2 is required for maintaining dormant cancer stem cell in hepatocellular carcinoma.

Project description:Cancer stem cells (CSCs) are responsible for therapy resistance and share several properties with normal stem cells. Here, we show that brain-expressed X-linked gene 2 (BEX2), which is essential for dormant CSCs in cholangiocarcinoma, is highly expressed in human hepatocellular carcinoma (HCC) lesions compared with the adjacent normal lesions and that in 41 HCC cases the BEX2high expression group is correlated with a poor prognosis. BEX2 localizes to Ki67-negative (nonproliferative) cancer cells in HCC tissues and is highly expressed in the dormant fraction of HCC cell lines. Knockdown of BEX2 attenuates CSC phenotypes, including sphere formation ability and aldefluor activity, and BEX2 overexpression enhances these phenotypes. Moreover, BEX2 knockdown increases cisplatin sensitivity, and BEX2 expression is induced by cisplatin treatment. Taken together, these data suggest that BEX2 induces dormant CSC properties and affects the prognosis of patients with HCC.

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