GATA3 interacts with and stabilizes HIF-1α to enhance cancer cell invasiveness

Lin, Mo‐Jun; Jin, Lin; Hsu, Chia‐Lang; Hf, Juan; Lou, Pei‐Jen; Huang, Min-Chuan

doi:10.1038/onc.2017.8

Cited by 63 publications

(38 citation statements)

References 37 publications

(41 reference statements)

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“… 23 In addition, GATA3 interacts with and stabilizes HIF-1α, which is important in the pathogenesis of various human cancers, and can enhance cancer cell invasiveness. 24 These data support the hypothesis that the GATA3 mutation identified in the present case is associated with her development of lung squamous cell carcinoma.…”

Section: Discussionsupporting

confidence: 90%

Lung squamous cell carcinoma associated with hypoparathyroidism with sensorineural deafness and renal dysplasia syndrome: a case report

Kojima

Nagano

Nakata

et al. 2018

OTT

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Hypoparathyroidism with sensorineural deafness and renal dysplasia (HDR) syndrome is an autosomal dominant condition caused by mutations of the gene encoding the dual zinc-finger transcription factor, GATA3. A previous study identified some patients with GATA3 gene variants and breast cancer, suggesting that GATA3 variants may contribute to tumorigenesis in estrogen receptor 1-positive breast tumors; however, these patients did not have HDR syndrome. A 32-year-old nonsmoking Japanese woman was histologically diagnosed with lung squamous cell carcinoma associated with HDR syndrome and a c.C952T>C (p.C318R) germline mutation in GATA3. This is the first report describing cancer in a patient with HDR syndrome. Our data indicates that GATA3 mutations may be a potential therapeutic target for lung cancer.

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Section: Discussionsupporting

confidence: 90%

Lung squamous cell carcinoma associated with hypoparathyroidism with sensorineural deafness and renal dysplasia syndrome: a case report

Kojima

Nagano

Nakata

et al. 2018

OTT

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“…GATA3 has been discovered to be linked with the development and invasion of cancer cells [54][55][56]. In this study, we identified GATA3 as a tumor suppressor gene that interacts with LINRIS.…”

Section: Discussionmentioning

confidence: 84%

LncRNA LINRIS stabilizes IGF2BP2 and promotes the aerobic glycolysis in colorectal cancer

et al. 2019

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Background: Long noncoding RNAs (lncRNAs) play nonnegligible roles in the epigenetic regulation of cancer cells. This study aimed to identify a specific lncRNA that promotes the colorectal cancer (CRC) progression and could be a potential therapeutic target. Methods:We screened highly expressed lncRNAs in human CRC samples compared with their matched adjacent normal tissues. The proteins that interact with LINRIS (Long Intergenic Noncoding RNA for IGF2BP2 Stability) were confirmed by RNA pull-down and RNA immunoprecipitation (RIP) assays. The proliferation and metabolic alteration of CRC cells with LINRIS inhibited were tested in vitro and in vivo.Results: LINRIS was upregulated in CRC tissues from patients with poor overall survival (OS), and LINRIS inhibition led to the impaired CRC cell line growth. Moreover, knockdown of LINRIS resulted in a decreased level of insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2), a newly found N 6 -methyladenosine (m 6 A) 'reader'. LINRIS blocked K139 ubiquitination of IGF2BP2, maintaining its stability. This process prevented the degradation of IGF2BP2 through the autophagy-lysosome pathway (ALP). Therefore, knockdown of LINRIS attenuated the downstream effects of IGF2BP2, especially MYC-mediated glycolysis in CRC cells. In addition, the transcription of LINRIS could be inhibited by GATA3 in CRC cells. In vivo experiments showed that the inhibition of LINRIS suppressed the proliferation of tumors in orthotopic models and in patient-derived xenograft (PDX) models.Conclusion: LINRIS is an independent prognostic biomarker for CRC. The LINRIS-IGF2BP2-MYC axis promotes the progression of CRC and is a promising therapeutic target.

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“…HIF-1α is critical for angiogenesis and new vascular formation, which is very important for tumor growth, metastasis and relapse (41). Therefore, HIF-1α may promote tumor progression and has been reported as a promising anticancer therapeutic target (42). Our previous studies also indicated that the downregulation of HIF-1α may mediate the anticancer activity of Evo in LoVo colon cancer cells (10).…”

Section: Discussionmentioning

confidence: 96%

BMP9 mediates the anticancer activity of evodiamine through HIF‑1α/p53 in human colon cancer cells

Huang

Cui

et al. 2019

Oncol Rep

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Colon cancer is one of the most common malignancies. Although there has been great development in treatment regimens over the last few decades, its prognosis remains poor. There is still a clinical need to find new drugs for colon cancer. Evodiamine (Evo) is a quinolone alkaloid extracted from the traditional herbal medicine plant Evodia rutaecarpa. In the present study, CCK-8, flow cytometry, reverse transcription quantitative polymerase chain reaction, western blot analysis and a xenograft tumor model were used to evaluate the anti-cancer activity of Evo in human colon cancer cells and determine the possible mechanism underlying this process. It was revealed that Evo exhibited prominent anti-proliferation and apoptosis-inducing effects in HCT116 cells. Bone morphogenetic protein 9 (BMP9) was notably upregulated by Evo in HCT116 cells. Exogenous BMP9 potentiated the anti-cancer activity of Evo, and BMP9 silencing reduced this effect. In addition, HIF-1α was also upregulated by Evo. The anticancer activity of Evo was enhanced by HIF-1α, but was reduced by HIF-1α silencing. BMP9 potentiated the effect of Evo on the upregulation of HIF-1α, and enhanced the antitumor effect of Evo in colon cancer, which was clearly reduced by HIF-1α silencing. In HCT116 cells, Evo increased the phosphorylation of p53, which was enhanced by BMP9 but reduced by BMP9 silencing. Furthermore, the effect of Evo on p53 was potentiated by HIF-1α and reduced by HIF-1α silencing. The present findings therefore strongly indicated that the anticancer activity of Evo may be partly mediated by BMP9 upregulation, which can activate p53 through upregulation of HIF-1α, at least in human colon cancer.

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GATA3 interacts with and stabilizes HIF-1α to enhance cancer cell invasiveness

Cited by 63 publications

References 37 publications

Lung squamous cell carcinoma associated with hypoparathyroidism with sensorineural deafness and renal dysplasia syndrome: a case report

Lung squamous cell carcinoma associated with hypoparathyroidism with sensorineural deafness and renal dysplasia syndrome: a case report

LncRNA LINRIS stabilizes IGF2BP2 and promotes the aerobic glycolysis in colorectal cancer

BMP9 mediates the anticancer activity of evodiamine through HIF‑1α/p53 in human colon cancer cells

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