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Your search keyword '"MARCH1"' showing total 3 results
Start Over Descriptor "MARCH1" Journal aging
3 results on '"MARCH1"'

1. Resveratrol inhibits the malignant progression of hepatocellular carcinoma via MARCH1-induced regulation of PTEN/AKT signaling

Author

Xia Wang, Peiyuan Wang, Xiucui Sun, Minjing Li, Wei Yang, Hanhan Dai, Mingdong Zhao, Jiaqi Su, Xuemei Hu, and Xu Wang

Subjects
Aging, Small interfering RNA, MARCH1, Carcinoma, Hepatocellular, endocrine system diseases, Carcinogenesis, Ubiquitin-Protein Ligases, Down-Regulation, Apoptosis, Resveratrol, resveratrol, medicine.disease_cause, survival, chemistry.chemical_compound, Mice, Downregulation and upregulation, Cell Movement, medicine, Tensin, PTEN, Animals, Humans, RNA, Small Interfering, Protein kinase B, Cell Proliferation, Gene knockdown, biology, Dose-Response Relationship, Drug, Chemistry, Liver Neoplasms, PTEN Phosphohydrolase, food and beverages, Cell Biology, Hep G2 Cells, hepatocellular carcinoma, PTEN/AKT, Xenograft Model Antitumor Assays, digestive system diseases, Gene Expression Regulation, Neoplastic, Gene Knockdown Techniques, biology.protein, Cancer research, Disease Progression, Female, Proto-Oncogene Proteins c-akt, Signal Transduction, Research Paper
Abstract

Resveratrol is a common, naturally occurring polyphenol confirmed with inhibited the cellular effects of carcinogenesis. However, the molecular mechanism underlying resveratrol's action against hepatocellular carcinoma (HCC) is still unclear. In addition, MARCH1 promotes the initiation and progression of HCC, but it is unclear whether resveratrol exerts antitumor efforts by regulating MARCH1 expression. This study determined the molecular mechanisms underlying the antitumor effects of resveratrol in HCC. Resveratrol induced apoptosis and inhibited the proliferation, migration, and invasion of HCC cell lines (HepG2 and Hep3B). In addition, it inhibited MARCH1 and phospho-protein kinase B (p-AKT) expression but upregulated the phosphatase and tensin homolog deleted on chromosome 10 (PTEN) dose-dependently both in vitro and in vivo. MARCH1 knockdown by small interfering RNA (siRNA) also increased PTEN expression. Meanwhile, MK2206 (an AKT inhibitor) and bisperoxovanadium (BPV; a PTEN inhibitor) combined with resveratrol decreased MARCH1 expression more than the single-treatment HCC group. These results suggested that resveratrol affects the biological characteristics of HCC via downregulation of MARCH1 expression.

Published
2019

2. Resveratrol inhibits the malignant progression of hepatocellular carcinoma via MARCH1-induced regulation of PTEN/AKT signaling.

Author

Dai H, Li M, Yang W, Sun X, Wang P, Wang X, Su J, Wang X, Hu X, and Zhao M

Subjects
Animals, Apoptosis drug effects, Carcinogenesis genetics, Carcinoma, Hepatocellular genetics, Carcinoma, Hepatocellular pathology, Cell Movement drug effects, Cell Movement genetics, Cell Proliferation drug effects, Cell Proliferation genetics, Disease Progression, Dose-Response Relationship, Drug, Down-Regulation drug effects, Female, Gene Expression Regulation, Neoplastic drug effects, Gene Knockdown Techniques, Hep G2 Cells, Humans, Liver Neoplasms genetics, Mice, PTEN Phosphohydrolase metabolism, Proto-Oncogene Proteins c-akt metabolism, RNA, Small Interfering metabolism, Resveratrol therapeutic use, Signal Transduction drug effects, Signal Transduction genetics, Ubiquitin-Protein Ligases genetics, Xenograft Model Antitumor Assays, Carcinogenesis drug effects, Carcinoma, Hepatocellular drug therapy, Liver Neoplasms drug therapy, Resveratrol pharmacology, Ubiquitin-Protein Ligases metabolism
Abstract

Resveratrol is a common, naturally occurring polyphenol confirmed with inhibited the cellular effects of carcinogenesis. However, the molecular mechanism underlying resveratrol's action against hepatocellular carcinoma (HCC) is still unclear. In addition, MARCH1 promotes the initiation and progression of HCC, but it is unclear whether resveratrol exerts antitumor efforts by regulating MARCH1 expression. This study determined the molecular mechanisms underlying the antitumor effects of resveratrol in HCC. Resveratrol induced apoptosis and inhibited the proliferation, migration, and invasion of HCC cell lines (HepG2 and Hep3B). In addition, it inhibited MARCH1 and phospho-protein kinase B (p-AKT) expression but upregulated the phosphatase and tensin homolog deleted on chromosome 10 (PTEN) dose-dependently both in vitro and in vivo. MARCH1 knockdown by small interfering RNA (siRNA) also increased PTEN expression. Meanwhile, MK2206 (an AKT inhibitor) and bisperoxovanadium (BPV; a PTEN inhibitor) combined with resveratrol decreased MARCH1 expression more than the single-treatment HCC group. These results suggested that resveratrol affects the biological characteristics of HCC via downregulation of MARCH1 expression.

Published
2020
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3. ciRs-6 upregulates March1 to suppress bladder cancer growth by sponging miR-653.

Author

Su Y, Feng W, Zhong G, Ya Y, Du Z, Shi J, Chen L, Dong W, and Lin T

Subjects
Animals, Cell Line, Tumor, Down-Regulation, Female, Humans, Mice, Mice, Nude, MicroRNAs genetics, Neoplasms, Experimental, RNA, Circular genetics, Ubiquitin-Protein Ligases genetics, Up-Regulation, Gene Expression Regulation, Neoplastic physiology, MicroRNAs metabolism, RNA, Circular metabolism, Ubiquitin-Protein Ligases metabolism, Urinary Bladder Neoplasms metabolism
Abstract

Background: Circular RNAs have been widely explored as potential biomarkers and therapeutic targets in bladder cancer; however, few have been functionally characterized., Results: ciRs-6 is expressed at low levels in cancer tissues and advanced tumor grades and stages, and its expression correlates with better outcomes for bladder cancer patients. In vitro and in vivo, ciRs-6 was shown to suppress bladder cancer growth by sponging miR-653 to elevate March1 levels. March1 is an E3 ubiquitin ligase that has been proven to suppress bladder cancer growth; knocking down March1 in ciRs-6 overexpressed bladder cancer cells reversed the tumor suppressive effect of ciRs-6., Conclusions: Our study identifies an oncogenic role of ciRs-6 and suggests its usefulness as a novel biomarker for bladder cancer diagnosis and prognosis and as a therapeutic target for bladder cancer., Methods: ciRs-6 was identified by RNA-seq and qPCR; CCK8 assays, clone forming assays and cell cycle analyses were performed to evaluate the in vitro effect of ciRs-6 in bladder cancer; further, a mouse subcutaneous tumor model was designed for in vivo analysis. RNA pulldown assays, miRNA capture experiments and dual luciferase assessments were applied for mechanistic studies.

Published
2019
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