ROCK1 promotes migration and invasion of non‑small‑cell lung cancer cells through the PTEN/PI3K/FAK pathway

Hu, Changpeng�; Liu, Yali; Huang, Jingbin�; Liu, Wuyi; Zhang, Qian; Tang, Qin; Sheng, Fangfang; Li, Guobing�; Zhang, Rong

doi:10.3892/ijo.2019.4864

Cited by 54 publications

(54 citation statements)

References 50 publications

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“…Next, we found that ROCK1 was a downstream target of miR‐340‐5p , which is consistent with data from a previous study 39 . ROCK1 is a member of the Rho‐associated protein kinase family and has a role in cell invasion in neoplasms 40 . ROCK1 is also overexpressed in several cancers, such as hepatocellular carcinoma, non‐small cell lung cancer, breast cancer and oral squamous cell carcinoma 41‐44 .…”

Section: Discussionsupporting

confidence: 90%

Long noncoding RNA LINC00346 promotes glioma cell migration, invasion and proliferation by up‐regulating ROCK1

Chen

et al. 2020

J Cellular Molecular Medi

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Long noncoding RNAs have key roles in glioma progression. However, the function and mechanisms of action of the long noncoding RNA, LINC00346, in glioma remain unclear. In our study, we observed that LINC00346 levels were increased in glioma tissue samples, and according to Gene Expression Profiling Interactive Analysis, its levels were related to disease‐free survival and overall survival rates, suggesting that a high level of LINC00346 expression corresponds to a poor prognosis. We next confirmed the high levels of LINC00346 expression in glioma tissues and cell lines and showed that LINC00346 knockdown suppressed glioma cell proliferation, migration and invasion; promoted apoptosis; and delayed tumour growth. Moreover, the oncogenic function of LINC00346 may be explained, in part, by the down‐regulation of miR‐340‐5p and the de‐repression of ROCK1. We showed that LINC00346 may function as a competing endogenous RNA of miR‐340‐5p, thereby de‐repressing ROCK1. This study revealed a new regulatory network in glioma and identified potential therapeutic targets for this cancer.

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Section: Discussionsupporting

confidence: 90%

Long noncoding RNA LINC00346 promotes glioma cell migration, invasion and proliferation by up‐regulating ROCK1

Chen

et al. 2020

J Cellular Molecular Medi

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“…[32][33][34] ROCK1 has been demonstrated to be upregulated in NSCLC and validated as a critical regulator of cancer genesis and progression. 35,36 Here, our results showed that ROCK1 was regulated by the KCNMB2-AS1/miR-374a-3p axis in NSCLC cells. Furthermore, increasing the activity of the miR-374a-3p/ROCK1 axis attenuated KCNMB2-AS1 silencing-induced inhibition of NSCLC progression.…”

mentioning

confidence: 54%

<p>Long Noncoding RNA KCNMB2-AS1 Increases ROCK1 Expression by Sponging microRNA-374a-3p to Facilitate the Progression of Non–Small-Cell Lung Cancer</p>

Huang

Wang

2020

CMAR

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Purpose The expression and roles of most long noncoding RNAs (lncRNAs) in non–small-cell lung cancer (NSCLC) remain poorly understood. Thus, this study investigated KCNMB2 antisense RNA 1 (KCNMB2-AS1) expression in NSCLC and determined the roles and mechanisms of KCNMB2-AS1 in regulating NSCLC progression. Methods KCNMB2-AS1 expression in NSCLC tissues and cells was detected using reverse transcription-quantitative polymerase chain reaction. Cell proliferation, apoptosis, migration, and invasion were evaluated using Cell Counting Kit-8, flow cytometry, Transwell migration, and Transwell invasion assays, respectively. In vivo tumor xenograft models were constructed to assess tumorigenicity. Bioinformatics predictions were performed to identify microRNAs targeting KCNMB2-AS1 . Interactions between KCNMB2-AS1 and miR-374a-3p were analyzed using RNA immunoprecipitation, luciferase reporter, and rescue experiments. Results KCNMB2-AS1 levels were increased in NSCLC tissues and cells. KCNMB2-AS1 silencing hindered NSCLC cell proliferation, migration, and invasion and promoted apoptosis in vitro. Additionally, KCNMB2-AS1 knockdown decreased tumor growth in vivo. Mechanistically, KCNMB2-AS1 functioned as an endogenous miR-374a-3p sponge and increased ρ-associated coiled-coil–containing protein kinase 1 (ROCK1) expression. Furthermore, increased miR-374a-3p/ROCK1 output attenuated KCNMB2-AS1 silencing-induced inhibition of NSCLC progression. Conclusion The KCNMB2-AS1/miR-374a-3p/ROCK1 pathway drives NSCLC progression, suggesting that this pathway can be targeted to reduce NSCLC progression.

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“…EGFR and its downstream signaling Ras/Raf/MEK/ERK and PI3K/Akt/mTOR pathways are strongly associated with human NSCLC [ 86 , 87 , 88 ]. The Ras/Raf/MEK/ERK and PI3K/Akt/mTOR signaling pathways crosstalk with the Hippo/YAP signaling pathway and negatively regulate Hippo kinases to activate the oncogenic function of YAP in cancer cells [ 89 , 90 , 91 , 92 ].…”

Section: Hippo/yap Singing Pathway In Nsclcmentioning

confidence: 99%

The Crosstalk between Src and Hippo/YAP Signaling Pathways in Non-Small Cell Lung Cancer (NSCLC)

Hsu

Yang

Jablons

et al. 2020

Cancers

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The advancement of new therapies, including targeted therapies and immunotherapies, has improved the survival of non-small-cell lung cancer (NSCLC) patients in the last decade. Some NSCLC patients still do not benefit from therapies or encounter progressive disease during the course of treatment because they have intrinsic resistance, acquired resistance, or lack a targetable driver mutation. More investigations on the molecular biology of NSCLC are needed to find useful biomarkers for current therapies and to develop novel therapeutic strategies. Src is a non-receptor tyrosine kinase protein that interacts with cell surface growth factor receptors and the intracellular signaling pathway to maintain cell survival tumorigenesis in NSCLC. The Yes-associated protein (YAP) is one of the main effectors of the Hippo pathway and has been identified as a promoter of drug resistance, cancer progression, and metastasis in NSCLC. Here, we review studies that have investigated the activation of YAP as mediated by Src kinases and demonstrate that Src regulates YAP through three main mechanisms: (1) direct phosphorylation; (2) the activation of pathways repressing Hippo kinases; and (3) Hippo-independent mechanisms. Further work should focus on the efficacy of Src inhibitors in inhibiting YAP activity in NSCLC. In addition, future efforts toward developing potentially reasonable combinations of therapy targeting the Src–YAP axis using other therapies, including targeted therapies and/or immunotherapies, are warranted.

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ROCK1 promotes migration and invasion of non‑small‑cell lung cancer cells through the PTEN/PI3K/FAK pathway

Cited by 54 publications

References 50 publications

Long noncoding RNA LINC00346 promotes glioma cell migration, invasion and proliferation by up‐regulating ROCK1

Long noncoding RNA LINC00346 promotes glioma cell migration, invasion and proliferation by up‐regulating ROCK1

<p>Long Noncoding RNA KCNMB2-AS1 Increases ROCK1 Expression by Sponging microRNA-374a-3p to Facilitate the Progression of Non–Small-Cell Lung Cancer</p>

The Crosstalk between Src and Hippo/YAP Signaling Pathways in Non-Small Cell Lung Cancer (NSCLC)

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