ID1 affects the efficacy of radiotherapy in glioblastoma through inhibition of DNA repair pathways

Guo, Qinhua; Guo, Ping; Mao, Qing; Jin, Lan; Lin, Yingying; Jiang, Jiyao; Qiu, Yongming

doi:10.1007/s12032-012-0325-6

Cited by 16 publications

(12 citation statements)

References 31 publications

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“…In addition, ID1 has been demonstrated to contribute to radioresistance in glioblastoma through inhibition of DNA repair pathways (34). The effect of ID1 knockdown on resistance to DDP in the GC cell lines MKN-28 and MGC-803 was examined.…”

Section: Resultsmentioning

confidence: 99%

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siRNA-mediated knockdown of ID1 disrupts Nanog- and Oct-4-mediated cancer stem cell-likeness and resistance to chemotherapy in gastric cancer cells

Wei

et al. 2017

Oncology Letters

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Abstract. DNA-binding protein inhibitor ID-1 (ID1) serves an essential role in tumor progression, and the self-renewal and pluripotency of embryonic stem cells. However, the effect of ID1 on the stemness and cancer stem cell (CSC)-like properties of gastric adenocarcinoma cells remains to be elucidated. In the present study, effective ID1 knockdown was achieved in gastric cancer (GC) cells using small interfering RNA, and the self-renewal ability and cisplatin (DDP) sensitivity of GC cells was subsequently examined. ID1 knockdown in the MKN-28 and MGC-803 cell lines was demonstrated to significantly suppress colony formation (P=0.005 in MKN-28 and P=0.001 in MGC-803), tumor spheroid formation (P=0.021 in MKN-28 and P=0.037 in MGC-803), cell proliferation (P=0.028 in MKN-28 and P=0.001 in MGC-803) and migration (P=0.002 in MKN-28 and P=0.015 in MGC-803). To the best of our knowledge, the present study revealed for the first time that ID1 knockdown suppresses the expression of the key CSC-associated factors Nanog and octamer-binding protein 4 (Oct-4). It was further demonstrated that ID1 knockdown sensitized GC cells to DDP. In conclusion, knockdown of ID1 attenuates the stem cell like-properties of self-renewal in normal GC cells, potentially through the targeting of Nanog and Oct-4, and subsequently decreases cell proliferation and resistance to DDP. The results of the present study suggest that ID1 functions as an oncogene in GC and regulates the stem cell like-properties of gastric cancer cells by targeting Nanog and Oct-4.

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Section: Resultsmentioning

confidence: 99%

“…Numerous studies have highlighted the complex role served by members of the ID subfamily in mammalian cell fate determination (21,27,28,34). IDs are involved in numerous biological processes, including the inhibition of differentiation, and the maintenance of self-renewal and multipotency in stem cells (22,23).…”

Section: Discussionmentioning

confidence: 99%

siRNA-mediated knockdown of ID1 disrupts Nanog- and Oct-4-mediated cancer stem cell-likeness and resistance to chemotherapy in gastric cancer cells

Wei

et al. 2017

Oncology Letters

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“…ID1 belongs to the basic helix-loop helix family of genes, which have been detected in multiple malignant tumors. In addition, the expression levels of these genes have been associated with invasive features of cancer (52,53). Increasing evidence has indicated that ID1 is upregulated in HCC samples and induces cellular proliferation.…”

Section: Ar and Inhibitor Of Differentiation 1 (Id1)mentioning

confidence: 99%

Androgen receptor in hepatocarcinogenesis: Recent developments and perspectives

et al. 2015

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Abstract. Previous studies have indicated that males are at a higher risk of developing hepatocellular carcinoma (HCC) compared with females. Identifying the factors that cause this gender-specific difference in the incidence of HCC has long been considered important for revealing the molecular mechanisms involved in hepatocarcinogenesis. Given the unprecedented tools that are now available for molecular research, genetic studies have established that the androgen receptor (AR) may be partly responsible for gender disparity in HCC. AR has a dual role, promoting HCC initiation and development, as well as suppressing HCC metastasis. The present review provides an overview of the involvement of AR signaling in HCC. The review highlighted important studies, examples of the direct AR transcriptional target genes involved in HCC and novel theories concerning the conventional concept, suggesting that targeting the AR, rather than the androgen, may provide an improved therapeutic approach for the treatment of HCC.

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“…And the inhibition of Id1 enhances the effect of temozolomide, delays tumor recurrence, and prolongs survival [32]. But an opposite conclusion was also acquired by Guo, Q et al who found that GBM patients with high Id1 expression had better survival than patients with low Id1 expression since Id1 expression could increase the radiotherapy efficacy [116]. Same conclusion was also obtained in a study of prostate cancer.…”

Section: Id1 In Therapeutic Resistancementioning

confidence: 85%

Inhibitor of Differentiation 1 (Id1) in Cancer and Cancer Therapy

Zhao

Gong

et al. 2020

Int. J. Med. Sci.

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The inhibitor of DNA binding (Id) proteins are regulators of cell cycle and cell differentiation. Of all Id family proteins, Id1 is mostly linked to tumorigenesis, cellular senescence as well as cell proliferation and survival. Id1 is a stem cell-like gene more than a classical oncogene. Id1 is overexpressed in numerous types of cancers and exerts its promotion effect to these tumors through different pathways. Briefly, Id1 was found significantly correlated with EMT-related proteins, K-Ras signaling, EGFR signaling, BMP signaling, PI3K/Akt signaling, WNT and SHH signaling, c-Myc signaling, STAT3 signaling, RK1/2 MAPK/Egr1 pathway and TGF-β pathway, etc. Id1 has potent effect on facilitating tumorous angiogenesis and metastasis. Moreover, high expression of Id1 plays a facilitating role in the development of drug resistance, including chemoresistance, radiation resistance and resistance to drugs targeting angiogenesis. However, controversial results were also obtained. Overall, Id1 represent a promising target of anti-tumor therapeutics based on its potent promotion effect to cancer. Numerous drugs were found exerting their anti-tumor function through Id1-related signaling pathways, such as fucoidan, berberine, tetramethylpyrazine, crizotinib, cannabidiol and vinblastine.

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ID1 affects the efficacy of radiotherapy in glioblastoma through inhibition of DNA repair pathways

Cited by 16 publications

References 31 publications

siRNA-mediated knockdown of ID1 disrupts Nanog- and Oct-4-mediated cancer stem cell-likeness and resistance to chemotherapy in gastric cancer cells

siRNA-mediated knockdown of ID1 disrupts Nanog- and Oct-4-mediated cancer stem cell-likeness and resistance to chemotherapy in gastric cancer cells

Androgen receptor in hepatocarcinogenesis: Recent developments and perspectives

Inhibitor of Differentiation 1 (Id1) in Cancer and Cancer Therapy

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