MiR-598 Suppresses Invasion and Migration by Negative Regulation of Derlin-1 and Epithelial-Mesenchymal Transition in Non-Small Cell Lung Cancer

Yang, Fengming; Wei, Ke; Qin, Zhiqiang; Liu, Weitao; Shao, Chao‐Peng; Wang, Chaoshan; Ma, Ling; Xie, Mengyan; Shu, Yongqian; Shen, Hua

doi:10.1159/000489803

Cited by 46 publications

(36 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This finding is in total agreement with an early report on the consistent detection of Vimentin expression in six cell lines explanted from COMM (including Shadow), a skin melanoma‐derived cell line and 28/29 tumour sections prepared from 11 COMM, 14 cutaneous and 4 digital canine melanomas . Vimentin is generally expressed by mesenchymal and neuroectodermal cells in normal tissue, and neoplastic cells that had undergone EMT in a high proportion of canine cancers . Along with Vimentin, tumour sections and primary cell lines consistently expressed biologically active MMP2 as revealed by IF and zymography.…”

Section: Discussionsupporting

confidence: 92%

Canine oral primary melanoma cells exhibit shift to mesenchymal phenotype and phagocytic behaviour

Schmid

Brodesser

Reifinger

et al. 2019

Vet Comparative Oncology

View full text Add to dashboard Cite

Canine oral malignant melanoma (COMM) is a potentially lethal cancer disease. We established primary cell lines from mostly amelanotic primary COMM and metastases and assessed lesions and derived cells for Melan A, PNL2 and CD146 expression. Then, migration and invasion of CD146‐enriched vs ‐depleted COMM cells were analysed. Epithelial‐to‐mesenchymal transition (EMT) was addressed by Vimentin‐staining and MMP2/MMP9 zymography. Phagocytic behaviour was analysed by histopathological examination and phagocytosis assay. While Melan A‐ and PNL2‐staining yielded inconsistent data, 100% of COMM sections and primary cells showed CD146 expression, suggesting that this protein may serve as a prognostic marker. An overall correlation between CD146‐expression and migration/invasion was not observed. All primary cell lines consistently expressed Vimentin and secreted biologically active MMP2, indicating that they had undergone EMT. Importantly, COMM sections exhibited cell‐in‐cell structures, and all primary cell lines exhibited phagocytic activity, supporting the concept that cell cannibalism may have a role in COMM progression.

show abstract

Section: Discussionsupporting

confidence: 92%

Canine oral primary melanoma cells exhibit shift to mesenchymal phenotype and phagocytic behaviour

Schmid

Brodesser

Reifinger

et al. 2019

Vet Comparative Oncology

View full text Add to dashboard Cite

show abstract

“…16 Inhibition of NSCLC cells growth and metastasis has been recognized as an effective treating strategy for NSCLC. Previous studies have demonstrated that a growing number of miRNAs played a role in the limiting tumor growth and EMT process in NSCLC, such as miR-206, 18 miR-598, 19 miR-126, 20 and miR-185. 17 EMT contributes a lot to tumor metastasis by changing tumor cells shape and improving the migratory and invasive capacities of tumor cells.…”

Section: Discussionmentioning

confidence: 99%

“…17 EMT contributes a lot to tumor metastasis by changing tumor cells shape and improving the migratory and invasive capacities of tumor cells. Previous studies have demonstrated that a growing number of miRNAs played a role in the limiting tumor growth and EMT process in NSCLC, such as miR-206, 18 miR-598, 19 miR-126, 20 and miR-185. 21 However, we for the first time, suggested that miR-105 was also one of the key regulators in modulating NSCLC cells EMT.…”

Section: Discussionmentioning

confidence: 99%

Retracted: MicroRNA‐105 promotes epithelial‐mesenchymal transition of nonsmall lung cancer cells through upregulating Mcl‐1

Jin

Qiang

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

Background A growing number of microRNAs have been proved to play significant roles in limiting tumor growth and the epithelial‐mesenchymal transition (EMT) process of nonsmall cell lung cancer (NSCLC). Present work aims to study the function of microRNA (miR)‐105 in EMT of NSCLC cells, which is unrevealed yet. Methods Two NSCLC cell lines A549 and Calu‐3 were transfected with miR‐105 mimic, inhibitor, or scrambled control. And then the effects of miR‐105 were evaluated by performing trypan blue staining, transwell assay, ANNEXIN‐FITC/propidium iodide (PI) double staining and Western blot analysis. The expression levels of myeloid cell leukemia‐1 (Mcl‐1) after transfection were tested by real‐time quantitative polymerase chain reaction and Western blot analysis. Whether Mcl‐1 was a downstream effector of miR‐105, and the involvement of mammalian target of Rapamycin (mTOR) and p38 mitogen‐activated protein kinase (p38MAPK) signaling pathways were assessed. Results The overexpression of miR‐105 significantly increased the viability and migration of A549 and Calu‐3, but had no impacts on cell apoptosis. Meanwhile, E‐cadherin was remarkably downregulated, and N‐cadherin, Vimentin, ZEB1, and Snail were upregulated by miR‐105 overexpression. Mcl‐1 was positively regulated by miR‐105, and the effects of miR‐105 overexpression on A549 and Calu‐3 cells viability, migration and EMT were all flattened by Mcl‐1 silence. Both mTOR and p38MAPK pathways were activated in miR‐105‐overexpressing and Mcl‐1‐overexpressing cells. Besides, inhibition of mTOR and p38MAPK pathways by using Rapamycin and VX‐702 abolished the regulatory effects of Mcl‐1 on EMT. Conclusion Our study underlines the importance of miR‐105 in modulating NSCLC cells EMT. miR‐105 promoted the EMT of NSCLC cells possibly via upregulation of Mcl‐1 and thereby activation of mTOR and p38MAPK signaling.

show abstract

“…Using CCK-8 and Transwell assays, it was revealed that miR-671-3p inhibited NSCLC cell proliferation and invasion. miRNAs have been demonstrated to target mRNAs for the regulation of gene expression in cancer (23). Through bioinformatics analysis, the present study identified that miR-671-3p may target CCND2.…”

Section: Discussionmentioning

confidence: 74%

miR‑671‑3p is downregulated in non‑small cell lung cancer and inhibits cancer progression by directly targeting CCND2

Yao

Zhou

2019

Mol Med Report

View full text Add to dashboard Cite

MicroRNAs (miRNAs) are implicated in the development and progression of non-small cell lung cancer (NSCLC). A previous study suggested that miR-671-3p suppresses the development of breast cancer. However, the role of miR-671-3p in NSCLC remains largely unknown. In the present study, it was identified that miR-671-3p was significantly upregulated in NSCLC tissues compared with adjacent normal tissues by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Similarly, decreased levels of miR-671-3p in NSCLC cell lines were observed compared with those in the non-tumorigenic human bronchial epithelial NL20 cell line. Cell Counting Kit-8 and Transwell invasion assays indicated that miR-671-3p overexpression suppressed the proliferation and invasion of A549 cells, and vice versa. Mechanistically, it was demonstrated that CCND2 was a direct target of miR-671-3p. RT-qPCR and western blot analysis indicated that miR-671-3p overexpression decreased the expression of CCND2 in A549 cells. Furthermore, rescue experiments demonstrated that the restoration of CCND2 may significantly reverse the suppressive roles of miR-671-3p overexpression on NSCLC cell proliferation and invasion. Taken together, the present study demonstrated that miR-671-3p exerted its tumor-suppressive roles via directly targeting CCND2 in NSCLC.

show abstract

MiR-598 Suppresses Invasion and Migration by Negative Regulation of Derlin-1 and Epithelial-Mesenchymal Transition in Non-Small Cell Lung Cancer

Cited by 46 publications

References 31 publications

Canine oral primary melanoma cells exhibit shift to mesenchymal phenotype and phagocytic behaviour

Canine oral primary melanoma cells exhibit shift to mesenchymal phenotype and phagocytic behaviour

Retracted: MicroRNA‐105 promotes epithelial‐mesenchymal transition of nonsmall lung cancer cells through upregulating Mcl‐1

miR‑671‑3p is downregulated in non‑small cell lung cancer and inhibits cancer progression by directly targeting CCND2

Contact Info

Product

Resources

About