Overexpressed KDM5B is associated with the progression of glioma and promotes glioma cell growth via downregulating p21

Dai, Bin; Hu, Zhiqiang; Huang, Hui; Zhu, Guangtong; Xiao, Zhiyong; Wan, Weiqing; Zhang, Peng; Jia, Wang; Zhang, Liwei

doi:10.1016/j.bbrc.2014.10.078

Cited by 43 publications

(39 citation statements)

References 33 publications

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“…This effect is maintained in hepatocellular cancer [6] and is also described in lung cancers via JARID1A [46]. JARID1A and JARID1B-mediated repression of other cdk inhibitors is also reported, including effects on p15, p16, and p21 [6, 12, 48, 49]. It remains unclear what contextual determinants dictate whether JARID1 proteins drive G 1 -S progression or promote arrest and senescence.…”

Section: Jarid1 Contribution To Cancer Progressionmentioning

confidence: 99%

JARID1 Histone Demethylases: Emerging Targets in Cancer

et al. 2017

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JARID1 proteins are histone demethylases that both regulate normal cell fates during development and contribute to the epigenetic plasticity that underlies malignant transformation. This H3K4 demethylase family participates in multiple repressive transcriptional complexes at promoters and has broader regulatory effects on chromatin that remain ill-defined. There is growing understanding of the oncogenic and tumor suppressive functions of JARID1 proteins, which are contingent on cell context and the protein isoform. Their contributions to stem cell-like de-differentiation, tumor aggressiveness, and therapy resistance in cancer have sustained interest in the development of JARID1 inhibitors. Here we review the diverse and context-specific functions of the JARID1 proteins that may impact the utilization of emerging targeted inhibitors of this histone demethylase family in cancer therapy.

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Section: Jarid1 Contribution To Cancer Progressionmentioning

confidence: 99%

JARID1 Histone Demethylases: Emerging Targets in Cancer

et al. 2017

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“…FAK, the focal adhesion kinase, functions as an oncogene involved in many cancers development and metastasis . P21, one of cell‐cycle inhibitors, mainly inhibits cell proliferation . Upregulation of FAK and downregulation of P21 have been reported in GC .…”

Section: Disscussionmentioning

confidence: 99%

Tumor-suppressive functions of long-chain acyl-CoA synthetase 4 in gastric cancer

Zhang

Wang

et al. 2016

IUBMB Life

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Long chain acyl CoA synthetase 4 (ACSL4) is a key enzyme in fatty acid metabolism with marked preference for arachidonic acid (AA). Recent reports have implicated its crucial roles in tumorigenesis. However in gastric cancer (GC), the expression and function of ACSL4 remain unclear. In the present study, we identified ACSL4 as a potential tumor suppressor in GC. The ACSL4 expression in GC samples was evaluated by realtime PCR and immunohistochemistry. The results indicated that the mRNA and protein levels of ACSL4 were frequently downregulated in cancer tissues compared with the adjacent non-cancerous mucosa control tissues. Cell-based functional assays exhibited that ectopic expression of ACSL4 inhibits cell growth, colony formation and cell migration, whereas ACSL4 knockdown enhanced these effects. In a nude mice model, ACSL4 knockdown also promoted subcutaneous xenografts' growth in vivo. Moreover, western blot analysis revealed that ACSL4 expression had a significant effect on FAK and P21 protein level. These findings suggest that ACSL4 plays a tumorsuppressive role and could be a potential therapeutic target in GC.

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“…Despite concerted worldwide efforts to tackle glioblastoma, patient prognosis remains grim and recurrence is inevitable (Rich, ; Stupp et al ., ). Several histone demethylases, including LSD1, KDM5A, and KDM5B, are upregulated in malignant gliomas, sustaining cell growth, and resistance to chemotherapy (Amente et al ., ; Banelli et al ., ; Black et al ., ; Dai et al ., ; Hayami et al ., ; Tzatsos et al ., ). In the present study, we examined the role of KDM2B in glioblastoma.…”

Section: Discussionmentioning

confidence: 99%

Targeting glioma stem‐like cell survival and chemoresistance through inhibition of lysine‐specific histone demethylase KDM2B

et al. 2018

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Glioblastoma (GBM) ranks among the most lethal cancers, with current therapies offering only palliation. Inter‐ and intrapatient heterogeneity is a hallmark of GBM, with epigenetically distinct cancer stem‐like cells (CSCs) at the apex. Targeting GSCs remains a challenging task because of their unique biology, resemblance to normal neural stem/progenitor cells, and resistance to standard cytotoxic therapy. Here, we find that the chromatin regulator, JmjC domain histone H3K36me2/me1 demethylase KDM2B, is highly expressed in glioblastoma surgical specimens compared to normal brain. Targeting KDM2B function genetically or pharmacologically impaired the survival of patient‐derived primary glioblastoma cells through the induction of DNA damage and apoptosis, sensitizing them to chemotherapy. KDM2B loss decreased the GSC pool, which was potentiated by coadministration of chemotherapy. Collectively, our results demonstrate KDM2B is crucial for glioblastoma maintenance, with inhibition causing loss of GSC survival, genomic stability, and chemoresistance.

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Overexpressed KDM5B is associated with the progression of glioma and promotes glioma cell growth via downregulating p21

Cited by 43 publications

References 33 publications

JARID1 Histone Demethylases: Emerging Targets in Cancer

JARID1 Histone Demethylases: Emerging Targets in Cancer

Tumor-suppressive functions of long-chain acyl-CoA synthetase 4 in gastric cancer

Targeting glioma stem‐like cell survival and chemoresistance through inhibition of lysine‐specific histone demethylase KDM2B

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