miR‐365 regulates liver cancer stem cells via RAC1 pathway

Jiang, Zongyuan; Ma, Bingqiang; Liu, Shaoguang; Li, Jing; Yang, Guangming; Hou, Yabo; Si, Ruohuang; Gao, Peng; Yan, Huiting

doi:10.1002/mc.22906

Cited by 40 publications

(25 citation statements)

References 40 publications

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“…The third SNP associated with serum PGII levels was rs121224 in miR-365b. This miRNA suppresses tumor cell growth and invasion of cancers such as breast cancer, hepatocarcinoma, small cell lung cancer, and GC [ 51 , 52 , 53 , 54 ]. In some tumors, serum miR-365 is a diagnostic or prognostic marker [ 54 , 55 , 56 , 57 ].…”

Section: Discussionmentioning

confidence: 99%

Polymorphisms in Pepsinogen C and miRNA Genes Associate with High Serum Pepsinogen II in Gastric Cancer Patients

Zorzi

Caggiari

et al. 2021

Microorganisms

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Background: Pepsinogen (PG) II (PGII) is a serological marker used to estimate the risk of gastric cancer but how PGII expression is regulated is largely unknown. It has been suggested that PGII expression, from the PGC (Progastricsin) gene, is regulated by microRNAs (miRNA), but how PGII levels vary with Helicobacter pylori (H. pylori) infection and miRNAs genotype remains unclear. Methods: Serum levels of PGI and PGII were determined in 80 patients with gastric cancer and persons at risk for gastric cancer (74 first-degree relatives of patients, 62 patients with autoimmune chronic atrophic gastritis, and 2 patients with dysplasia), with and without H. pylori infection. As control from the general population, 52 blood donors were added to the analyses. Associations between PGII levels and genetic variants in PGC and miRNA genes in these groups were explored based on H. pylori seropositivity and the risk for gastric cancer. The two-dimensional difference in gel electrophoresis (2D-DIGE) and the NanoString analysis of messenger RNA (mRNAs) from gastric cancer tissue were used to determine the pathways associated with increased PGII levels. Results: PGII levels were significantly higher in patients with gastric cancer, and in those with H. pylori infection, than in other patients or controls. A PGI/PGII ratio ≤ 3 was found better than PGI < 25 ng/mL to identify patients with gastric cancer (15.0% vs. 8.8%). For two genetic variants, namely rs8111742 in miR-Let-7e and rs121224 in miR-365b, there were significant differences in PGII levels between genotype groups among patients with gastric cancer (p = 0.02 and p = 0.01, respectively), but not among other study subjects. Moreover, a strict relation between rs9471643 C-allele with H. pylori infection and gastric cancer was underlined. Fold change in gene expression of mRNA isolated from gastric cancer tissue correlated well with polymorphism, H. pylori infection, increased PGII level, and pathway for bacteria cell entry into the host. Conclusions: Serum PGII levels depend in part on an interaction between H. pylori and host miRNA genotypes, which may interfere with the cut-off of PGI/PGII ratio used to identify persons at risk of gastric cancer. Results reported new findings regarding the relation among H. pylori, PGII-related host polymorphism, and genes involved in this interaction in the gastric cancer setting.

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Section: Discussionmentioning

confidence: 99%

Polymorphisms in Pepsinogen C and miRNA Genes Associate with High Serum Pepsinogen II in Gastric Cancer Patients

Zorzi

Caggiari

et al. 2021

Microorganisms

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“…Ras-related C3 botulinum toxin substrate 1 (RAC1) is also a subfamily of the Ras superfamily, which mediates intercellular adhesion, cell cycle, and epithelial differentiation [ 96 ]. Upregulation of miR-194 and miR-365 targeting RAC1 inhibits liver CSCs expansion, leading to the increased sensitivity to sorafenib and cisplatin [ 97 , 98 ]. In addition to regulating the complicated signals, miRNAs are able to diminish the number of CSCs more directly—targeting the hallmarks of CSCs.…”

Section: Mirna-mediated Emt and Cscs In Chemotherapy Resistancementioning

confidence: 99%

MiRNA-mediated EMT and CSCs in cancer chemoresistance

Dong

Zhu

et al. 2021

Exp Hematol Oncol

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Cancer stem cells (CSCs) are a small group of cancer cells, which contribute to tumorigenesis and cancer progression. Cancer cells undergoing epithelial-to-mesenchymal transition (EMT) acquire the chemoresistant ability, which is regarded as an important feature of CSCs. Thus, there emerges an opinion that the generation of CSCs is considered to be driven by EMT. In this complex process, microRNAs (miRNAs) are found to play a key role. In order to overcome the drug resistance, inhibiting EMT as well as CSCs phenotype seem feasible. Thereinto, regulating the EMT- or CSCs-associated miRNAs is a crucial approach. Herein, we conduct this review to elaborate on the complicated interplay between EMT and CSCs in cancer chemoresistance, which is modulated by miRNAs. In addition, we elucidate the therapeutic strategy to overcome drug resistance through targeting EMT and CSCs.

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“…While knockdown of miR-25 enhanced the sensitivity of LCSCs to TNF-related apoptosis inducing ligand (TRAIL)-mediated apoptosis via the phosphatase and tensin homologue (PTEN)/PI3K/Akt/Bad signaling pathway ( Feng et al, 2016 ). miR-365 directly regulated Ras-related C3 botulinum toxin substrate 1 (RAC1) by binding with the mRNA 3′UTR and affected HCC drug resistance ( Jiang et al, 2019 ). In addition, miR-486 directly targeted sirtuin1, which exhibits high expression in self-renewing and tumorigenic LCSCs ( Yan et al, 2019 ).…”

Section: The Role and Classification Of Ncrnasmentioning

confidence: 99%

Recent Advances in Liver Cancer Stem Cells: Non-coding RNAs, Oncogenes and Oncoproteins

Zhu

2020

Front. Cell Dev. Biol.

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Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies worldwide, with high morbidity, relapse, metastasis and mortality rates. Although liver surgical resection, transplantation, chemotherapy, radiotherapy and some molecular targeted therapeutics may prolong the survival of HCC patients to a certain degree, the curative effect is still poor, primarily because of tumor recurrence and the drug resistance of HCC cells. Liver cancer stem cells (LCSCs), also known as liver tumor-initiating cells, represent one small subset of cancer cells that are responsible for disease recurrence, drug resistance and death. Therefore, understanding the regulatory mechanism of LCSCs in HCC is of vital importance. Thus, new studies that present gene regulation strategies to control LCSC differentiation and replication are under development. In this review, we provide an update on the latest advances in experimental studies on non-coding RNAs (ncRNAs), oncogenes and oncoproteins. All the articles addressed the crosstalk between different ncRNAs, oncogenes and oncoproteins, as well as their upstream and downstream products targeting LCSCs. In this review, we summarize three pathways, the Wnt/β-catenin signaling pathway, phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway, and interleukin 6/Janus kinase 2/signal transducer and activator of transcription 3 (IL6/JAK2/STAT3) signaling pathway, and their targeting gene, c-Myc. Furthermore, we conclude that octamer 4 (OCT4) and Nanog are two important functional genes that play a pivotal role in LCSC regulation and HCC prognosis.

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miR‐365 regulates liver cancer stem cells via RAC1 pathway

Cited by 40 publications

References 40 publications

Polymorphisms in Pepsinogen C and miRNA Genes Associate with High Serum Pepsinogen II in Gastric Cancer Patients

Polymorphisms in Pepsinogen C and miRNA Genes Associate with High Serum Pepsinogen II in Gastric Cancer Patients

MiRNA-mediated EMT and CSCs in cancer chemoresistance

Recent Advances in Liver Cancer Stem Cells: Non-coding RNAs, Oncogenes and Oncoproteins

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