MicroRNA‐7‐5p induces cell growth inhibition, cell cycle arrest and apoptosis by targeting PAK2 in non‐small cell lung cancer

Li, Qin; Wu, Xingping; Guo, Lin; Shi, Jun; Li, Jiashu

doi:10.1002/2211-5463.12738

Cited by 46 publications

(29 citation statements)

References 33 publications

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“…For example, Du et al (34) demonstrated that miR-335-3p expression is downregulated in NSCLC tissues compared with normal tissues. Furthermore, downregulated miR-7-5p expression has been reported in NSCLC tissues and cell lines, which exerts regulatory effects on tumor cell biological processes (35). Overexpression of miR-100 in NSCLC tissues has been demonstrated to predict the poor prognosis of this malignancy (36).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of miR‑518b in non‑small cell lung cancer serves as a biomarker and facilitates tumor cell proliferation, migration and invasion

Zhang

Gong

et al. 2020

Oncol Lett

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Several microRNAs (miRNA/miR) have been reported to serve critical roles in tumorigenesis. The present study aimed to investigate miR-518b expression in non-small cell lung cancer (NSCLC), and determine its clinical significance and biological function in this malignancy. Reverse transcription-quantitative PCR was performed to assess miR-518b expression in NSCLC. The diagnostic value of miR-518b was determined via a receiver operating characteristic curve, while its prognostic value was assessed using the Kaplan-Meier method. Gain-and loss-of-function experiments were performed to determine the functional role of miR-518b in NSCLC progression. The results demonstrated that miR-518b expression was upregulated in NSCLC serum, tissues and cell lines compared with the corresponding normal controls. Furthermore, high miR-518b expression was significantly associated with larger tumor size, lymph node metastasis and advanced TNM stage, as well as poor overall survival in patients with NSCLC. Serum miR-518b expression was identified as a candidate diagnostic biomarker for NSCLC, with sensitivity of 88.1% and specificity of 81.7%. Furthermore, the cell experiments indicated that NSCLC cell proliferation, migration and invasion were enhanced following overexpression of miR-518b; however, these effects were reversed following miR-518b knockdown. Taken together, the results of the present study suggest that elevated miR-518b expression in NSCLC serves a potential oncogenic role by facilitating tumor cell proliferation, migration and invasion, and thus may serve as a candidate diagnostic and prognostic biomarker.

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Section: Discussionmentioning

confidence: 99%

Overexpression of miR‑518b in non‑small cell lung cancer serves as a biomarker and facilitates tumor cell proliferation, migration and invasion

Zhang

Gong

et al. 2020

Oncol Lett

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“…Cells are harvested at indicated times and treated with Accumax to obtain a single cell suspension. Propidium iodide staining was completed as described (13). Cells were analyzed on a FACscan Flow Cytometer (Becton Dickensen) and cell cycle distribution determined using ModFit LT 2.0 software (Verity Software House).…”

Section: Cell Cyclementioning

confidence: 99%

Beyond Conventional Models: Recreating the Initiation, Evolution, and Genome of GBM

Böhm

DePetro

Binding

et al. 2019

Preprint

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Background: Imagining ways to prevent or treat glioblastoma (GBM) have been hindered by a lack of understanding of its pathogenesis. Although PDGF-AA overexpression may be an early event, critical details of the core biology are lacking. Existing PDGF-driven models replicate its microscopic appearance but not the genomic architecture characteristic of the human disease.Here we report a new model of GBM that overcomes this barrier to authenticity. Methods:Using a method developed to study neural stem cells, we investigated the effects of PDGF-AA on subventricular zone (SVZ) cells, the putative cell of origin of GBM. We micro-dissected SVZ tissue from p53-null and wild-type adult mice, established primary cultures in media supplemented with PDGF-AA, and assessed cell viability, proliferation, genome stability, and tumour forming potential. Results: Counterintuitive to its canonical role as a growth factor, we observed immediate and massive death of SVZ cells in PDGF-AA. Wild-type cells did not survive in PDGF-AA. However, a small fraction of null cells evaded apoptosis, displayed attenuated proliferation, gradually accumulated whole chromosome gains and losses, and, signalled by sudden rapid proliferation and growth factor independence, became tumorigenic in immune-competent syngeneic mice. Transformed cells had an OPC-like profile, were resistant to PDGFR-α inhibition, and harboured highly abnormal karyotypes similar to those seen in human GBMs. Conclusion: This model associates genome instability in SVZ cells with chronic exposure to PDGF-AA; it is the first model to replicate the genomic landscape of GBM and first in which the earliest phases of GBM can be directly observed. IMPORTANCE OF STUDYWe have developed a mouse model in which the initiation, evolution and genomic landscape of GBM can be thoroughly studied thus paving the way for ideas about how this deadly brain cancer might be prevented, interrupted at an occult stage, or treated with very different therapies.

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“…MiR-143-3p serves as a tumor suppressor via modulating the growth, invasion and epithelial-mesenchymal transition (EMT) by regulating KH Domain Containing RNA Binding-5 (QKI-5) in esophageal squamous cell carcinoma [ 10 ]. MiRNA-7-5p inhibits cell growth, induces cell cycle arrest and cell apoptosis via modulating Paired Box 2 (PAX2) in non-small cell lung cancer (NSCLC) [ 11 ]. In ovarian cancer, miRNA-141 enhances the anoikis resistance of metastatic ovarian carcinoma cell by regulating Kruppel Like Factor 12/Sp1 Transcription Factor (KLF12/Sp1) axis [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Tumor-suppressor miRNA-27b-5p regulates the growth and metastatic behaviors of ovarian carcinoma cells by targeting CXCL1

et al. 2020

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Background MicroRNAs (miRNAs) play crucial functions in the progression of ovarian cancer. MicroRNA-27b-5p (miR-27b-5p) has been identified as a cancer-associated miRNA. Nevertheless, the expression profile of miR-27b-5p and its functions in ovarian cancer are unexplored. Methods qRT-PCR and western blot analysis were used to detect the levels of miR-27b-5p and C-X-C motif chemokine ligand 1 (CXCL1). The impact of miR-27b-5p on ovarian cancer cells proliferation, migration and invasion in vitro were investigated using Cell Counting Kit-8 (CCK8), wound healing and Transwell, respectively. The expression of matrix metalloprotein-2/9 (MMP-2/9) were measured using immunofluorescence staining. Bioinformatics and luciferase reporter analysis were used to predict the target of miR-27b-5p. The growth of ovarian cancer cells in vivo was evaluated using transplanted tumor model. Results Here, we demonstrated that miR-27b-5p was downregulated in ovarian carcinoma cells and clinical specimens. Higher expression of miR-27b-5p was associated with an unfavorable overall survival in patients with ovarian cancer. Upregulation of miR-27b-5p decreased the viability, migration ability and invasion capacity of SKOV3 and OVCAR3 cell. MiR-27b-5p also inhibited the growth of SKOV3 cell in nude mice. Additionally, we verified that CXCL1 was a target of miR-27b-5p in ovarian carcinoma cells. Restoring the expression of CXCL1 abolished the inhibitory impacts of miR-27b-5p in ovarian cancer carcinoma cells. Conclusion This research revealed that miR-27b-5p restrained the progression of ovarian carcinoma possibly via targeting CXCL1.

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MicroRNA‐7‐5p induces cell growth inhibition, cell cycle arrest and apoptosis by targeting PAK2 in non‐small cell lung cancer

Cited by 46 publications

References 33 publications

Overexpression of miR‑518b in non‑small cell lung cancer serves as a biomarker and facilitates tumor cell proliferation, migration and invasion

Overexpression of miR‑518b in non‑small cell lung cancer serves as a biomarker and facilitates tumor cell proliferation, migration and invasion

Beyond Conventional Models: Recreating the Initiation, Evolution, and Genome of GBM

Tumor-suppressor miRNA-27b-5p regulates the growth and metastatic behaviors of ovarian carcinoma cells by targeting CXCL1

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