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BHLHE40 modulates gene transcription in breast cancer cells exposed to hypoxia and low glucose

ABSTRACT: BHLHE40 modulates gene transcription in breast cancer cells exposed to hypoxia and low glucose

PROVIDER: PRJNA419652 | ENA |

REPOSITORIES: ENA

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BHLHE40 modulates gene transcription in breast cancer cells exposed to hypoxia and low glucose

Project description:Knockdown of BHLHE40 expression significantly reduced primary tumor growth and spontaneous lung metastasis in an orthotopic xenograft model of human breast cancer. Gene expression analysis implicated a role of BHLHE40 in hypoxia-induced exosomic secretion of Heparin Binding Epidermal Growth Factor HBEGF, which promotes cell survival and invasion. BHLHE40 induces HBEGF transcription by blocking DNA binding of HDAC1 and HDAC2.

2018-10-30 | GSE107300 | GEO

BHLHE40 is key hypoxia-induced transcriptional repressor in beta cells

Project description:To assess the impact of hypoxia on global gene expression of beta cells, we performed bulk RNA-seq on mouse islets, human islets and MIN6 cells. Bhlhe40 was transcriptional repressor which was highly induced by hypoxia in beta cells. Thus, we established Bhlhe40 overexpressing MIN6 cells and performed RNA-seq to identify the targets of Bhlhe40.

2023-05-01 | GSE202603 | GEO

Hypoxia-responsive interaction between Cyclin T1, BHLHE40, and Tim8-Tim13 regulates RNA Polymerase II

Project description:P-TEFb regulates the pause release checkpoint on transcription by RNA Polymerase II. We sought hypoxia-specific interactions that could direct PTEF-b activity to hypoxia-responsive genes. Using a biochemical purification approach, we discovered a hypoxia-specific, chromatin-associated interaction between the P-TEFb subunit Cyclin T1 (CCNT1), the mitochondrial chaperone Tim8-Tim13 complexes, and the hypoxia-inducible, DNA-binding transcription factor BHLHE40. This interaction is conserved across diverse cell line models. Tim8-Tim13 complex disruption and BHLHE40 silencing both impair the transcriptional response to acute hypoxia by RNAPII in DLD-1 cells. HIF is not involved in the CCNT1/BHLHE40/Tim8-Tim13 interaction, and BHLHE40 expression is not entirely HIF-dependent: neither genetic HIF-1β knockout nor pharmacological inhibition of HIF-2α using belzutifan eliminates BHLHE40. Finally, BHLHE40 depletion compromises the proliferation of 786-O clear cell renal carcinoma cells, which constitutively express HIF-2α and hypoxia-responsive genes. Together, these findings reveal a HIF-independent regulatory axis in which Tim8a-Tim13 complexes and BHLHE40 that modulate PTEF-b activity in the transcriptional response to hypoxia.

2026-04-10 | GSE293152 | GEO

Expression data from mouse differentiated Bhlhe40-GFPneg and Bhlhe40-GFPpos TH17 cells

Project description:Microarray data on TH17 cells from Bhlhe40-GFP reporter mice We used microarrays to detail the global programme of gene expression in polarized Bhlhe40-GFPneg and Bhlhe40-GFPpos TH17 cells Purified naÃ¯ve CD4 T cells from spleen were polarized under TH17 condition in vitro. On day 4, cells were stimulated with PMA and ionomycin, and sorted by their Bhlhe40-GFP expression prior to microarray analysis

2016-01-04 | E-GEOD-75407 | biostudies-arrayexpress

BHLHE40 is key hypoxia-induced transcriptional repressor in beta cells

Project description:BHLHE40 is key hypoxia-induced transcriptional repressor in beta cells

| PRJNA836763 | ENA

Expression data from mouse differentiated Bhlhe40-GFPneg and Bhlhe40-GFPpos TH17 cells

2016-01-04 | GSE75407 | GEO

The BHLHE40‒PPM1F‒AMPK pathway regulates energy metabolism and is associated with the aggressiveness of endometrial cancer

Project description:BHLHE40 is a basic helix-loop-helix transcription factor that is involved in multiple cell activities including differentiation, cell cycle, and epithelial-to-mesenchymal transition. While there is growing evidence to support the functions of BHLHE40 in energy metabolism, little is known about the mechanism. In this study, we found that BHLHE40 expression was downregulated in cases of endometrial cancer of higher grade and advanced disease. Knockdown of BHLHE40 in endometrial cancer cells resulted in suppressed oxygen consumption and enhanced extracellular acidification. Suppressed pyruvate dehydrogenase (PDH) activity and enhanced lactated dehydrogenase (LDH) activity was observed in the knockdown cells. Knockdown of BHLHE40 also led to dephosphorylation of AMPKα Thr172 and enhanced phosphorylation of PDHA1 Ser293 and LDHA Tyr10. These results suggested that BHLHE40 modulates PDH and LDH activity by regulating the phosphorylation status of PDHA1 and LDHA. We found that BHLHE40 enhanced AMPKα phosphorylation by directly suppressing the transcription of an AMPKα-specific phosphatase, PPM1F. Our immunohistochemical study showed that the expression of BHLHE40, PPM1F, and phosphorylated AMPKα correlated with the prognosis of endometrial cancer patients. Because AMPK is a central regulator of energy metabolism in cancer cells, targeting the BHLHE40‒PPM1F‒AMPK axis may represent a strategy to control cancer development.

2023-09-04 | GSE241941 | GEO

STAT4 promotes Bhlhe40 induction to drive protective IFN-g from natural killer cells during viral infection [BHLHE40 CUT&RUN]

Project description:NK cells represent a cellular component of the mammalian innate immune system, and mount rapid responses against viral infection, including the secretion of the potent anti-viral effector cytokine IFN-g. Following mouse cytomegalovirus (MCMV) infection, Bhlhe40 was the most highly induced transcription factor in NK cells among the basic helix-loop-helix family. Bhlhe40 upregulation in NK cells depended upon IL-12 and IL-18 signals, with the promoter of Bhlhe40 enriched for STAT4 and the permissive histone H3K4me3, and STAT4-deficient NK cells showing an impairment of Bhlhe40 induction and diminished H3K4me3. Transcriptomic and protein analysis of Bhlhe40-deficient NK cells revealed a defect in IFN-g production during MCMV infection, resulting in diminished protective immunity following viral challenge. Finally, we provide evidence that Bhlhe40 directly promotes IFN-g by binding throughout the Ifng loci in activated NK cells. Thus, our study reveals how STAT4-mediated control of Bhlhe40 drives protective IFN-g secretion by NK cells during viral infection.

2023-09-13 | GSE242900 | GEO

Hypoxia-responsive interaction between Cyclin T1, BHLHE40, and Tim8-Tim13 regulates RNA Polymerase II

Project description:Hypoxia-responsive interaction between Cyclin T1, BHLHE40, and Tim8-Tim13 regulates RNA Polymerase II

| PRJNA1242900 | ENA

LRRFIP2 modulates the response to hypoxia during embryonic cardiogenesis

Project description:LRRFIP2 modulates the response to hypoxia during embryonic cardiogenesis

| PRJNA844233 | ENA