MiR-320a effectively suppresses lung adenocarcinoma cell proliferation and metastasis by regulating STAT3 signals

Lv, Qing; Hu, Jinxia; Li, Youjie; Xie, Ning; Song, Dandan; Zhao, Wei; Yan, Yun‐Fei; Li, Baosheng; Wang, Pingyu; Xie, Songqiang

doi:10.1080/15384047.2017.1281497

Cited by 63 publications

(50 citation statements)

References 33 publications

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“…17,18 In this regard, several miRNAs have been reported to suppress or promote lung cancer cell survival or death. [19][20][21][22] Consistent with these reports, we have previously reported that miR-886-3Pwas associated with survival of SCL. 23 In the current study, we further investigated role of miR-886-3P in regulating small cell lung caner cell proliferation, migration, colony formation, mesenchymal-epithelial transition (MET), and in vivo xenograft tumor formation and growth.…”

Section: Introductionsupporting

confidence: 85%

MicroRNA-886-3P functions as a tumor suppressor in small cell lung cancer

Shen

Zhou

et al. 2018

Cancer Biology & Therapy

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Small cell lung cancer (SCLC) is a highly aggressive disease and miRNAs may play an important role in modulating SCLC progression. We have previously screened 924 miRNAs and found that miR-886-3P was negatively associated with SCLC survival. In the current study, we further investigated the role of miR-886-3P mimic in regulating SCLC cell phenotypic alteration in vitro and xenograft tumor formation in vivo. We found that transfection of miR-886-3P mimic significantly inhibited SCLC cell proliferation, migration, and colony formation, and induced mesenchymal-epithelial transition (MET) by suppressing TGF-ß1 synthesis in vitro. Furthermore, intra-tumor injection of miR-886-3P mimic lead to necrosis and suppression of tumor invasion to the surrounding tissue in the subcutaneous xenograft tumor, and intra-vein injection of miR-886-3P mimic suppressed xenograft lung cancer growth in vivo. These findings suggested that miR-886-3P functions as a tumor suppressor in SCLC and thus, it might be a potential therapeutic molecule in the treatment of lung cancer.

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Section: Introductionsupporting

confidence: 85%

MicroRNA-886-3P functions as a tumor suppressor in small cell lung cancer

Shen

Zhou

et al. 2018

Cancer Biology & Therapy

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“…Recent works demonstrated the role of mir‐320a as tumor suppressor in NSCLC by directly regulating IGF‐1R or VDAC1 expression suggesting this miRNA as a potential therapeutic target. Furthermore, mir‐320a was also involved in lung metastasis formation through down‐regulation of STAT3 and NRP‐1 . Here describe a novel role of mir‐320a in the cross‐talk among immune cells in lung microenvironment to promote tumor growth.…”

Section: Discussionmentioning

confidence: 84%

Circulating mir‐320a promotes immunosuppressive macrophages M2 phenotype associated with lung cancer risk

Fortunato

Borzi

Milione

et al. 2019

Intl Journal of Cancer

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miRNAs play a central role in the complex signaling network of cancer cells with the tumor microenvironment. Little is known on the origin of circulating miRNAs and their relationship with the tumor microenvironment in lung cancer. Here, we focused on the cellular source and relative contribution of different cell types to circulating miRNAs composing our risk classifier of lung cancer using in vitro/in vivo models and clinical samples. A cell‐type specific expression pattern and topography of several miRNAs such as mir‐145 in fibroblasts, mir‐126 in endothelial cells, mir‐133a in skeletal muscle cells was observed in normal and lung cancer tissues. Granulocytes and platelets are the major contributors of miRNAs release in blood. miRNAs modulation observed in plasma of lung cancer subjects was consistent with de‐regulation of the same miRNAs observed during immunosuppressive conversion of immune cells. In particular, activated neutrophils showed a miRNA profile mirroring that observed in plasma of lung cancer subjects. Interestingly mir‐320a secreted by neutrophils of high‐risk heavy‐smokers promoted an M2‐like protumorigenic phenotype through downregulation of STAT4 when shuttled into macrophages. These findings suggest a multifactorial and nonepithelial cell‐autonomous origin of circulating miRNAs associated with risk of lung cancer and that circulating miRNAs may act in paracrine signaling with causative role in lung carcinogenesis and immunosuppression.

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“…MiR‐320a has been identified in a number of studies largely as an inhibitor of oncogenesis, including cell proliferation, metastasis and chemoresistance. In 2017, Lv et al demonstrated that miR‐320a suppressed lung adenocarcinoma cell proliferation and metastasis and enhanced irradiation‐induced apoptosis by regulating signal transduced and activator of transcription 3. Furthermore, in 2014, Gao et al screened differentially expressed miRNAs in primary gastrointestinal stromal tumour patients and imatinib‐resistant patients, finding that miR‐320a down‐regulation was highly associated with chemoresistance.…”

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA AFAP1‐AS1/miR‐320a/RBPJ axis regulates laryngeal carcinoma cell stemness and chemoresistance

Yuan

Cheng

Song

et al. 2018

J Cellular Molecular Medi

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AFAP1‐AS1 is a long non‐coding RNA that is associated with tumorigenesis and poor prognosis in a variety of cancers. We have been suggested that AFAP1‐AS1 increases tumorigenesis in laryngeal carcinoma specifically by enhancing stemness and chemoresistance. We assessed AFAP1‐AS1 expression in human laryngeal specimens, paired adjacent normal tissues and human HEp‐2 cells. Indeed, we found not only that AFAP1‐AS1 was up‐regulated in laryngeal carcinoma specimens and cells, but also that stemness‐associated genes were overexpressed. Silencing of AFAP1‐AS1 promoted HEp‐2 cell chemoresistance under cisplatin treatment. Expression of AFAP1‐AS1 was increased in drug‐resistant Hep‐2 cells. We then probed the mechanism of AFAP1‐AS1 activity and determined that miR‐320a was a potential molecular target of AFAP1‐AS1. Luciferase reporter and qRT‐PCR assays of AFAP1‐AS1 and miR‐320a levels in human specimens and cell cultures indicated that AFAP1‐AS1 negatively regulates miR‐320a. To discover the molecular mechanism of miR‐320a, we again used the DIANA Tools algorithm to predict its genetic target, RBPJ. After cloning the 3′‐untranslated regions (3′‐UTR) of RBPJ into a luciferase reporter, we determined that miR‐320a did in fact reduce RBPJ mRNA and protein levels. Ultimately, we determined that AFAP1‐AS1 increases RBPJ expression by negatively regulating miR‐320a and RBPJ overexpression rescues stemness and chemoresistance inhibited by AFAP1‐AS1 silencing. Taken together, these results suggest that AFAP1‐AS1 can serve as a prognostic biomarker in laryngeal carcinoma and that miR‐320a has the potential to improve standard therapeutic approaches to the disease, especially for cases in which cancer cell stemness and drug resistance present significant barriers to effective treatment.

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MiR-320a effectively suppresses lung adenocarcinoma cell proliferation and metastasis by regulating STAT3 signals

Cited by 63 publications

References 33 publications

MicroRNA-886-3P functions as a tumor suppressor in small cell lung cancer

MicroRNA-886-3P functions as a tumor suppressor in small cell lung cancer

Circulating mir‐320a promotes immunosuppressive macrophages M2 phenotype associated with lung cancer risk

Long non‐coding RNA AFAP1‐AS1/miR‐320a/RBPJ axis regulates laryngeal carcinoma cell stemness and chemoresistance

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