MiR-22-silenced Cyclin A Expression in Colon and Liver Cancer Cells Is Regulated by Bile Acid Receptor

Yang, Fan; Ying, Haoqiang; Liu, Hui‐Xin; Wan, Yu‐Jui Yvonne

doi:10.1074/jbc.m114.620369

Cited by 69 publications

(74 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Deregulation of cyclin A2 was associated with erroneous cell proliferation and chromosomal instability (38,39), and aberrant expression of cyclin A2 has been linked to multiple types of malignancies, including breast, liver, and lung cancers (38)(39)(40). In light of our observation that USP7-mediated deubiquitination and stabilization of PHF8 regulate the expression of cyclin A2, it is reasonable to postulate that the USP7/PHF8 signaling pathway plays a role in cell proliferation and carcinogenesis.…”

Section: Resultsmentioning

confidence: 93%

Stabilization of histone demethylase PHF8 by USP7 promotes breast carcinogenesis

Wang¹,

Ma²,

Song³

et al. 2016

Journal of Clinical Investigation

159

175

View full text Add to dashboard Cite

Section: Resultsmentioning

confidence: 93%

Stabilization of histone demethylase PHF8 by USP7 promotes breast carcinogenesis

Wang¹,

Ma²,

Song³

et al. 2016

Journal of Clinical Investigation

159

175

View full text Add to dashboard Cite

“…Accumulating amounts of evidence suggest that miR-22-3p partcipates mainly in cell growth and differentiation. Previous studies have shown that miR-22-3p can promote CLL-B cell and cardiomyocytes proliferation [26,27]; however, in most carcinomas, including breast cancer [28], gastric carcinoma [29], medulloblastomas [30] and liver cancer [31], miR-22-3p suppressed cancer cell proliferation. Thus the biological functions of miR-22-3p in HASMCs require further study.…”

Section: Cellular Physiology and Biochemistry Cellular Physiology Andmentioning

confidence: 99%

Mir-22-3p Inhibits Arterial Smooth Muscle Cell Proliferation and Migration and Neointimal Hyperplasia by Targeting HMGB1 in Arteriosclerosis Obliterans

Huang¹,

Wang

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

Background: Aberrant vascular smooth muscle cell (VSMC) proliferation and migration contribute to the development of vascular pathologies, such as atherosclerosis and postangioplasty restenosis. The aim of this study was to determine whether miR-22-3p plays a role in regulating human artery vascular smooth muscle cell (HASMC) function and neointima formation. Methods: Quantitative real-time PCR (qRT-PCR) and fluorescence in situ hybridization (FISH) were used to detect miR-22-3p expression in human arteries. Cell Counting and EdU assays were performed to assess cell proliferation, and transwell and wound closure assays were performed to assess cell migration. Moreover, luciferase reporter assays were performed to identify the target genes of miR-22-3p. Finally, a rat carotid artery balloon-injury model was used to determine the role of miR-22-3p in neointima formation. Results: MiR-22-3p expression was downregulated in arteriosclerosis obliterans (ASO) arteries compared with normal arteries, as well as in platelet-derived growth factor-BB (PDGF-BB)-stimulated HASMCs compared with control cells. MiR-22-3p overexpression had anti-proliferative and anti-migratory effects and dual-luciferase assay showed that high mobility group box-1 (HMGB1) is a direct target of miR-22-3p in HASMCs. Furthermore, miR-22-3p expression was negatively correlated with HMGB1 expression in ASO tissue specimens. Finally, LV-miR-22-3p-mediated miR-22-3p upregulation significantly suppressed neointimal hyperplasia specifically by reducing HMGB1 expression in vivo. Conclusions: Our results indicate that miR-22-3p is a

show abstract

“…For example, the miR-22 shows different effects in these cancers [80][81][82][83]. DADS can silence HIF-1α (hypoxia inducible factor 1α) via increasing expression of miR-22 to repress VEGF (vascular endothelial growth factor) expression to block angiogenesis, leading to the disruption of cancer progression [79,84]. The upregulation of miR-22 induced by DADS may post-transcriptionally target cyclin A2 and CDKN1A (cyclin-dependent kinase inhibitor 1A) to arrest the cell cycle in G0/G1 phage in CRC and liver cancer cells, respectively [85,86].…”

Section: Regulation Of the Mirnas By Dadsmentioning

confidence: 99%

The Progress of Diallyl Disulfide in Anti-Cancer

Lz¹,

Liao²,

Wang³

et al. 2017

Chemotherapy

View full text Add to dashboard Cite

Considerable evidence in recent years suggests that garlic has anti-proliferative effects on various types of cancer. Garlic contains water-soluble and oil-soluble sulfur compounds. Oil-soluble compounds (OSCs), such as diallyl sulfide (DAS), diallyl disulfide (DADS), diallyl trisulfide (DATS) and ajoene are more effective than watersoluble compounds in protection against cancer. DADS, a major organosulfur compound derived from garlic, can reduce carcinogen-induced cancers in experimental animals and inhibit the proliferation of various types of cancer cells. The mechanisms of these action of DADS include activation of metabolic enzymes that detoxify carcinogens, suppression of the formation of DNA adducts, antioxidant effects, regulation of cell-cycle progression, induction of apoptosis, and inhibition of angiogenesis and metastasis. These topics are discussed in depth in this review.

show abstract

MiR-22-silenced Cyclin A Expression in Colon and Liver Cancer Cells Is Regulated by Bile Acid Receptor

Cited by 69 publications

References 35 publications

Stabilization of histone demethylase PHF8 by USP7 promotes breast carcinogenesis

Stabilization of histone demethylase PHF8 by USP7 promotes breast carcinogenesis

Mir-22-3p Inhibits Arterial Smooth Muscle Cell Proliferation and Migration and Neointimal Hyperplasia by Targeting HMGB1 in Arteriosclerosis Obliterans

The Progress of Diallyl Disulfide in Anti-Cancer

Contact Info

Product

Resources

About