HES5 promotes cellular proliferation of non-small cell lung cancer through STAT3 signaling

Gu, Shudong; Zhang, Rui; J, Gu; Li, Xia; Lv, Liting; Jiang, Jingting; Xu, Zhen; Wang, Shuo; Shi, Cui; Wang, Danping; Wu, Changping

doi:10.3892/or.2016.5268

Cited by 7 publications

(8 citation statements)

References 25 publications

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“…Western blot analysis. Protein extraction and western blot analysis were performed as previously described [18]. The band intensity was measured by an ImageJ analysis system.…”

Section: Methodsmentioning

confidence: 99%

CtBP2 promotes proliferation and reduces drug sensitivity in non-small cell lung cancer via the Wnt/β-catenin pathway

Wang

Xue

et al. 2018

neo

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The C-terminal binding protein 2 (CtBP2) is crucial for the activation of the Wnt/β-catenin pathway and regulates significant cellular processes in multiple cancer cells. However, the role of CtBP2 in non-small cell lung cancer (NSCLC) remains uncertain. Our western blotting and immunohistochemistry assays revealed that CtBP2 expression was obviously increased in NSCLC tissues and cells. In addition, the chi-square test and Kaplan-Meier analysis showed that over-expression of CtBP2 correlates with more invasive tumor phenotype and poor prognosis. In vitro studies with serum starvation-refeeding and CtBP2-shRNA transfection assay demonstrated that CtBP2 expression facilitates NSCLC cell proliferation and reduces sensitivity to cis-diamminedichloroplatinum (CDDP). The possible signaling transduction pathways were investigated, and the immunoprecipitation assay revealed that CtBP2 interacts directly with DvL1. Depletion of CtBP2 resulted in inhibited DvL1 expression and decreased expression of downstream genes. Moreover, our study showed that CtBP2 knockdown enhanced NSCLC cell sensitivity to CDDP through inhibition of the Wnt/β-catenin pathway. These results suggest that CtBP2 plays a crucial role in NSCLC progression and CDDP sensitivity, and that CtBP2 depletion can provide a new target for NSCLC treatment.

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“…Western blot analysis. Protein extraction and western blot analysis were performed as previously described [18]. The band intensity was measured by an ImageJ analysis system.…”

Section: Methodsmentioning

confidence: 99%

CtBP2 promotes proliferation and reduces drug sensitivity in non-small cell lung cancer via the Wnt/β-catenin pathway

Wang

Xue

et al. 2018

neo

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“…RNA seq revealed increased transcripts of the Notch3 target genes, HES5 and Hey2. HES5 has been shown to increase activation of STAT3 and STAT3 promotes glioblastoma stem cell renewal [ 24 , 41 ], and acts synergistically with Nanog to maintain pluripotency of embryonic stem cells [ 42 ]. In addition, we also found increased STAT3 expression by both splice variants.…”

Section: Discussionmentioning

confidence: 99%

The estrogen receptor variants β2 and β5 induce stem cell characteristics and chemotherapy resistance in prostate cancer through activation of hypoxic signaling

et al. 2018

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Chemotherapy resistant prostate cancer is a major clinical problem. When the prostate cancer has become androgen deprivation resistant, one of the few treatment regimens left is chemotherapy. There is a strong connection between a cancer’s stem cell like characteristics and drug resistance. By performing RNA-seq we observed several factors associated with stem cells being strongly up-regulated by the estrogen receptor β variants, β2 and β5. In addition, most of these factors were also up-regulated by hypoxia. One mechanism of chemotherapy resistance was expression of the hypoxia-regulated, drug transporter genes, where especially ABCG2 and MDR1 were shown to be expressed in recurrent prostate cancer and to cause chemotherapy resistance by efficiently transporting drugs like docetaxel out of the cells. Another mechanism was expression of the hypoxia-regulated Notch3 gene, which causes chemotherapy resistance in urothelial carcinoma, although the mechanism is unknown. It is well known that hypoxic signaling is involved in increasing chemotherapy resistance. Regulation of the hypoxic factors, HIF-1α and HIF-2α is very complex and extends far beyond hypoxia itself. We have recently shown that two of the estrogen receptor β variants, estrogen receptor β2 and β5, bind to and stabilize both HIF-1α and HIF-2α proteins leading to expression of HIF target genes. This study suggests that increased expression of the estrogen receptor β variants, β2 and β5, could be involved in development of a cancer’s stem cell characteristics and chemotherapy resistance, indicating that targeting these factors could prevent or reverse chemotherapy resistance and cancer stem cell expansion.

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“…HES5 is involved in neural stem cell maintenance, regulating mammalian neuronal differentiation and neuronal stem cell self-renewal (7,8). It is also implicated in cell differentiation and elevating tumorigenesis in cancers including prostate, nonsmall-cell lung, ovarian ,liver, and neuroblastoma (8)(9)(10)(11)(12). According to these studies, HES5 may play a role in the onset and progression of cancers.…”

Section: Introductionmentioning

confidence: 99%

NOTCH Target Gene HES5 Distinct Anti-Tumorigenic Roles in Gastric Carcinoma

Farmad

Chamanian

Alimardani

et al. 2021

Preprint

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I. Background:Gastric cancer (GC) is ranked the third greatest cause of mortality globally and the second common cancer in Iran. To date, many pathways including HES family have been found to be linked to cellular proliferation, differentiation and cancer. HES5, a transcription factor that binds to DNA, is known as a downstream protein in Notch pathway. Therefore, we aimed to investigate the association between HES5 expression and GC.II. Methods and Results:In this study,75 gastric cancer patients were included. After RNA extraction and cDNA synthesis, the expression rate of HES5 was evaluated by quantitative Real-time PCR. Also, presence of H. Pylori infection was verified using specific primers set for H. pylori, and PCR on extracted DNA. The results showed a remarkable decrease in HES level in malignant tissues when compared to the neighboring non-cancerous tissues (Normal) (P< 0.0001). Moreover, an inverse relation between down regulation of HES 5 gene and H.Pylori infection was identified. In conclusionIII. Conclusions: These findings emphasize that HES5 may notably suppress the tumor development.

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HES5 promotes cellular proliferation of non-small cell lung cancer through STAT3 signaling

Cited by 7 publications

References 25 publications

CtBP2 promotes proliferation and reduces drug sensitivity in non-small cell lung cancer via the Wnt/β-catenin pathway

CtBP2 promotes proliferation and reduces drug sensitivity in non-small cell lung cancer via the Wnt/β-catenin pathway

The estrogen receptor variants β2 and β5 induce stem cell characteristics and chemotherapy resistance in prostate cancer through activation of hypoxic signaling

NOTCH Target Gene HES5 Distinct Anti-Tumorigenic Roles in Gastric Carcinoma

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