SNF2H promotes hepatocellular carcinoma proliferation by activating the Wnt/β-catenin signaling pathway

Wang, Yanan; Qin, Juanxiu; Liu, Qian; Hong, Xufen; Li, Tianming; Zhu, Yuanjun; He, Lei; Zheng, Bing

doi:10.3892/ol.2016.4681

Cited by 12 publications

(12 citation statements)

References 33 publications

(33 reference statements)

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“…The imitation switch nuclear ATPase SMARCA5 (Snf2h) is one of the most conserved chromatin remodeling factors. SMARCA5 expression is upregulated in many aggressive tumors (20)(21)(22)(23)(24)(25), several studies have indicated signi cantly higher expression of SMARCA5 in tumor tissues compared with adjacent normal tissues, including hepatocellular carcinoma (19), gastric cancer (21), and prostate cancer (6). Our research is consistent with the previous reports.…”

Section: Discussionsupporting

confidence: 90%

“…Some study showed that SMARCA5 depletion in breast cancer cells could inhibit invasion with MMP2 downregulation (20). Wang etal reported that overexpression of SMARCA5 in BEL-7402 cells improved the cell growth and knockdown of SMARCA5 expressionin in Huh7 cells inhibited cell growth (19). Others showed that SMARCA5 Deletion Inhibited proliferation of myeloblasts and affected function of normal stem cells (22).…”

Section: Discussionmentioning

confidence: 99%

“…SMARCA5 is an oncogene in various types of tumors. Studies have shown that SNF2H can promote the growth and proliferation of liver cancer cells (19). At the same time, SMARCA5 is associated with poor prognosis of breast cancer patients and can promote the proliferation and invasion of breast cancer cells (20).…”

Section: Introductionmentioning

confidence: 99%

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High SMARCA5 Expression is Associated With Poor Prognosis in Patients With Non-Small Cell Lung Cancer

Yang¹,

Wen²,

Li³

et al. 2020

Preprint

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Background: SMARCA5 has been proved to play the role of oncogene in various types of tumors. The purpose of our study was to study the relationship between the expression of SMARCA5 and the prognosis of patients with Non-small cell lung cancer(NSCLC), and to investigate the effect of silencing the expression of SMARCA5 on the biological behavior of NSCLC. Methods：Immunohistochemistry method was adopted to detect to the expressions of SMARCA5 proteins in NSCLC and normal lung tissues. The correlation between the expression of SMARCA5 and clinicopathological factors and survival prognosis of patients with NSCLC were analyzed by statistical methods. Western blot and RT-PCR were used to detect the expression of SMARCA5 in normal human bronchial epithelial cell line (HBE) and human lung cancer cell lines (A549, Lu165, SK-MES-1 and NCI-H520). SMARCA5 siRNA was employed to silence the the expression of SMARCA5. MTT and Transwell methods were used to detect the proliferation and invasion of lung cancer cells.Results: SMARCA5 protein were highly expressed in 78 (59.5%) NSCLC tissues. SMARCA5 mRNA (P<0.05) and protein (P<0.05) were significantly higher in NSCLC tissues than in the adjacent normal tissues. SMARCA5 expression was significantly associated with poorly differentiation (P<0.001), advanced TNM stage (P<0.001), and pleural invasion (P=0.032). Meanwhile, High expression of SMARCA5 was associated with poor prognosis of NSCLC patients. Knockdown of SMARCA5 expression inhibited cell growth and invasion in NSCLC. Conclusion: High expression of SMARCA5 is associated with poor prognosis in patients with NSCLC, and SMARCA5 can increase activity of proliferation and invasion in NSCLC cells. SMARCA5 may play a decisive role in tumorigenesis of NSCLC.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

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High SMARCA5 Expression is Associated With Poor Prognosis in Patients With Non-Small Cell Lung Cancer

Yang¹,

Wen²,

Li³

et al. 2020

Preprint

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“…S3f). CHD3 efficiently repositions the nucleosome to the edge of the dsDNA 15,17,19). This can be also seen on physiological templates such as drosophila HSP70 promotor or mouse rDNA promotor (Fig.…”

Section: While Adp Comparably Inhibits the Atp Hydrolysis Rate Of Chd3 And Snf2h Snf2hdependent Nucleosome Remodeling Is Preferentially Imentioning

confidence: 66%

Sequence and functional differences in the ATPase domains of CHD3 and SNF2H promise potential for selective regulability and drugability

et al. 2021

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Chromatin remodelers use the energy of ATP hydrolysis to regulate chromatin dynamics. Their impact for development and disease requires strict enzymatic control. Here, we address the differential regulability of the ATPase domain of hSNF2H and hCHD3, exhibiting similar substrate affinities and enzymatic activities. Both enzymes are comparably strongly inhibited in their ATP hydrolysis activity by the competitive ATPase inhibitor ADP. However, the nucleosome remodeling activity of SNF2H is more strongly affected than that of CHD3. Beside ADP, also IP 6 inhibits the nucleosome translocation of both enzymes to varying degrees, following a competitive inhibition mode at CHD3, but not at SNF2H. Our observations are further substantiated by mutating conserved Q-and Kresidues of ATPase domain motifs. The variants still bind both substrates and exhibit a wild-type similar, basal ATP hydrolysis. Apart from three CHD3 variants, none of the variants can translocate nucleosomes, suggesting for the first time that the basal ATPase activity of CHD3 is sufficient for nucleosome remodeling. Together with the ADP data, our results propose a more efficient coupling of ATP hydrolysis and remodeling in CHD3. This aspect correlates with findings that CHD3 nucleosome translocation is visible at much lower ATP concentrations than SNF2H. We propose sequence differences between the ATPase domains of both enzymes as an explanation for the functional differences and suggest that aa interactions, including the conserved Q-and K-residues distinctly regulate ATPase-dependent functions of both proteins. Our data emphasize the benefits of remodeler ATPase domains for selective drugability and/or regulability of chromatin dynamics.

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“…Increased in gastric cancer [156], breast cancer [157], and liver cancer [158]. Activated Wnt/β-catenin signaling [158] and promoted cancer cell proliferation, colony formation and invasion [157,158]. Depletion in HeLa cells led to apoptotic phenotype [154].…”

Section: Smarca5 Snf2h) *mentioning

confidence: 99%

The Emerging Roles of ATP-Dependent Chromatin Remodeling Complexes in Pancreatic Cancer

Hasan

Ahuja

2019

Cancers

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Pancreatic cancer is an aggressive cancer with low survival rates. Genetic and epigenetic dysregulation has been associated with the initiation and progression of pancreatic tumors. Multiple studies have pointed to the involvement of aberrant chromatin modifications in driving tumor behavior. ATP-dependent chromatin remodeling complexes regulate chromatin structure and have critical roles in stem cell maintenance, development, and cancer. Frequent mutations and chromosomal aberrations in the genes associated with subunits of the ATP-dependent chromatin remodeling complexes have been detected in different cancer types. In this review, we summarize the current literature on the genomic alterations and mechanistic studies of the ATP-dependent chromatin remodeling complexes in pancreatic cancer. Our review is focused on the four main subfamilies: SWItch/sucrose non-fermentable (SWI/SNF), imitation SWI (ISWI), chromodomain-helicase DNA-binding protein (CHD), and INOsitol-requiring mutant 80 (INO80). Finally, we discuss potential novel treatment options that use small molecules to target these complexes.

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SNF2H promotes hepatocellular carcinoma proliferation by activating the Wnt/β-catenin signaling pathway

Cited by 12 publications

References 33 publications

High SMARCA5 Expression is Associated With Poor Prognosis in Patients With Non-Small Cell Lung Cancer

High SMARCA5 Expression is Associated With Poor Prognosis in Patients With Non-Small Cell Lung Cancer

Sequence and functional differences in the ATPase domains of CHD3 and SNF2H promise potential for selective regulability and drugability

The Emerging Roles of ATP-Dependent Chromatin Remodeling Complexes in Pancreatic Cancer

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