Serum response factor (SRF) promotes ROS generation and hepatic stellate cell activation by epigenetically stimulating NCF1/2 transcription

Kong, Ming; Chen, Xuyang; Lv, Fangqiao; Ren, Haozhen; Fan, Zhiwen; Qin, Hao; Yu, Liming; Shi, Xiaolei; Xu, Yong

doi:10.1016/j.redox.2019.101302

Cited by 52 publications

(46 citation statements)

References 77 publications

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“…SRF has been proposed to regulate the hepatic stellate cells. 32,33 Moreover, SRF and myocyte enhancer factor-2 worked collaboratively to modulate the expression of muscle-specific genes, such as miR-133a. 34 The myocardin-related transcription factors A and B-SRF pathway is of great significance for cell proliferation, motility, and adhesion, which were all major processes underlying the progression of cancers.…”

Section: Discussionmentioning

confidence: 99%

<p>SRF Potentiates Colon Cancer Metastasis and Progression in a microRNA-214/PTK6-Dependent Manner</p>

Li¹,

Wan²,

Su³

et al. 2020

CMAR

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Serum response factor (SRF), a sequence-specific transcription factor, is closely related to metastasis of gastric cancer, a digestive tract cancer. Herein, we probed the effect of SRF on metastasis and progression of colon cancer (CC), another digestive tract disorder, and the detailed mechanism. Methods: Microarray analysis was conducted on tumor and adjacent tissues to filter differentially expressed miRNA, followed by RT-qPCR validation in CC cell lines. The transcription factor and the target gene of microRNA-214 (miR-214) were predicted, and their binding relationships were tested by luciferase reporter assays and ChIP assays. Subsequently, SRF and protein tyrosine kinase 6 (PTK6) expression in CC patients and cells was evaluated by RT-qPCR, while JAK2 and STAT3 expression in cells by Western blot analysis. To further explore functions of miR-214, PTK6 and SRF on CC, CC cells were delivered with si-PTK6, miR-214 mimic and/or SRF overexpression. Results: miR-214 expressed poorly in CC tissues and cell lines, which related to advanced TNM staging and survival. miR-214 mimic inhibited proliferation, migration, invasion, xenograft tumor growth and metastasis of CC cells. SRF, overexpressed in CC samples and cells, suppressed the transcription of miR-214. Meanwhile, SRF upregulation counteracted the inhibitory role of miR-214 mimic in CC cell growth. miR-214 negatively regulated PTK6 expression to impair the JAK2/STAT3 pathway activation, thereby halting CC cell proliferation, migration, invasion, xenograft tumor growth and metastasis. Conclusion: Altogether, miR-214 may perform as a tumor suppressor in CC, and the SRF/ miR-214/PTK6/JAK2/STAT3 axis could be applied as a biomarker and potential therapeutic target.

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Section: Discussionmentioning

confidence: 99%

<p>SRF Potentiates Colon Cancer Metastasis and Progression in a microRNA-214/PTK6-Dependent Manner</p>

Li¹,

Wan²,

Su³

et al. 2020

CMAR

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“…NCF1 encodes the regulatory subunits of the NADPH oxidase complex, p47phox (Kong et al, 2019). NCF1-derived ROS play an important role in liver fibrosis and loss of NCF1 function in mice results in resistant to liver fibrosis (Bataller et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

The Target MicroRNAs and Potential Underlying Mechanisms of Yiqi-Bushen-Tiaozhi Recipe against‐Non-Alcoholic Steatohepatitis

Wang

Cai

et al. 2020

Front. Pharmacol.

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MicroRNAs (miRNAs) have emerged as potential therapeutic targets for non-alcoholic fatty liver disease/non-alcoholic steatohepatitis (NAFLD/NASH). Traditional Chineses Medicine (TCM) plays an important role in the prevention or treatment of NAFLD/NASH. However, miRNA targets of TCM against NASH still remain largely unknown. Here, we showed that Yiqi-Bushen-Tiaozhi (YBT) recipe effectively attenuated diet-induced NASH in C57BL/6 mice. To identify the miRNA targets of YBT and understand the potential underlying mechanisms, we performed network pharmacology using miRNA and mRNA deep sequencing data combined with Ingenuity Pathway Analysis (IPA). Mmu-let-7a-5p, mmu-let-7b-5p, mmu-let-7g-3p and mmu-miR-106b-3p were screened as the main targets of YBT. Our results suggested that YBT might alleviate NASH by regulating the expression of these miRNAs that potentially modulate inflammation/immunity and oxidative stress. This study provides useful information for guiding future studies on the mechanism of YBT against NASH by regulating miRNAs.

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“…Chromatin Immunoprecipitation (ChIP) assays were performed essentially as described before 47,[66][67][68][69][70][71][72][73][74][75][76][77][78][79][80] . In brief, chromatin in control and treated cells were cross-linked with 1% formaldehyde for 8 min at room temperature, and then sequentially washed with ice-cold phosphate-buffered saline, Solution I (10 mM HEPES, pH 7.5, 10 mM EDTA, 0.5 mM EGTA, 0.75% Triton X-100), and Solution II (10 mM HEPES, pH 7.5, 200 mM NaCl, 1 mM EDTA, 0.5 mM EGTA).…”

Section: Chromatin Immunoprecipitation (Chip)mentioning

confidence: 99%

Epigenetic activation of the small GTPase TCL contributes to colorectal cancer cell migration and invasion

et al. 2020

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TC10-like (TCL) is a small GTPase that has been implicated in carcinogenesis. Elevated TCL expression has been observed in many different types of cancers although the underlying epigenetic mechanism is poorly understood. Here we report that TCL up-regulation was associated with high malignancy in both human colorectal cancer biopsy specimens and in cultured colorectal cancer cells. Hypoxia, a pro-metastatic stimulus, up-regulated TCL expression in HT-29 cells. Further studies revealed that myocardin-related transcription factor A (MRTF-A) promoted migration and invasion of HT-29 cells in a TCL-dependent manner. MRTF-A directly bound to the proximal TCL promoter in response to hypoxia to activate TCL transcription. Chromatin immunoprecipitation (ChIP) assay showed that hypoxia stimulation specifically enhanced acetylation of histone H4K16 surrounding the TCL promoter, which was abolished by MRTF-A depletion or inhibition. Mechanistically, MRTF-A interacted with and recruited the H4K16 acetyltransferase hMOF to the TCL promoter to cooperatively regulate TCL transcription. hMOF depletion or inhibition attenuated hypoxia-induced TCL expression and migration/invasion of HT-29 cells. In conclusion, our data identify a novel MRTF-A-hMOF-TCL axis that contributes to colorectal cancer metastasis.

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Serum response factor (SRF) promotes ROS generation and hepatic stellate cell activation by epigenetically stimulating NCF1/2 transcription

Cited by 52 publications

References 77 publications

<p>SRF Potentiates Colon Cancer Metastasis and Progression in a microRNA-214/PTK6-Dependent Manner</p>

<p>SRF Potentiates Colon Cancer Metastasis and Progression in a microRNA-214/PTK6-Dependent Manner</p>

The Target MicroRNAs and Potential Underlying Mechanisms of Yiqi-Bushen-Tiaozhi Recipe against‐Non-Alcoholic Steatohepatitis

Epigenetic activation of the small GTPase TCL contributes to colorectal cancer cell migration and invasion

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