&lt;p&gt;miR-31 Modulates Liver Cancer HepG2 Cell Apoptosis and Invasion via ROCK1/F-Actin Pathways&lt;/p&gt;

Zhang, Xin; Xu, Lan; Yang, Ting

doi:10.2147/ott.s227467

Cited by 22 publications

(16 citation statements)

References 52 publications

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“…We have also made some extensions to the present study. Previous studies have found that F-actin was involved in cell proliferation and motility, and its homeostasis could be regulated by ROCK1 (ROCK1 depolymerized F-actin) [38]. In the present study, ROCK1 expression was found to hamper F-actin expression, and miR-30b-3p was an upstream effector of ROCK1/F-actin.…”

Section: Discussionsupporting

confidence: 55%

LncRNA BCYRN1 promotes cell migration and invasion of non-small cell lung cancer via the miR-30b-3p/ROCK1 axis

Song¹,

Wei-gang²,

Zhu³

et al. 2022

neo

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Long non-coding RNA brain cytoplasmic RNA 1 (LncRNA BCYRN1) has been proved to participate in the cancer cell metastasis process, including non-small cell lung cancer (NSCLC).However, the underlying molecular mechanisms involved in the BCYRN1-mediated function remain largely unknown. The qRT-PCR analysis was carried out to examine the relative expressions of BCYRN1, microRNA-30b-3p (miR-30b-3p), and Rho-associated coiled-coil protein kinase 1 (ROCK-1). ROCK1 protein level was detected via western blot assay. The migrative and invasive abilities of H520 and A549 cells were evaluated via Transwell assay. The relationships between BCYRN1 and miR-30b-3p or ROCK-1 and miR-30b-3p were examined by luciferase reporter assay.The expression levels of BCYRN1 and ROCK1 were upregulated in NSCLC tissues and ce lls, while miR-30b-3p was downregulated. Higher BCYRN1 expression indicated lymph node metastasis and advanced tumor-node-metastasis (TNM) stage of NSCLC patients. Loss of BCYRN1 suppressed cell migration and invasion. More importantly, miR-30b-3p possessed the binding sites with BCYRN1. Besides, BCYRN1 negatively regulated the expression level of miR-30b-3p. Meanwhile, ROCK-1 was proven to be directly targeted by miR-30b-3p. In addition, the silencing of miR-30b-3p also weakened the effect of BCYRN1 knockdown on cell migration and invasion. In vivo, BCYRN1 silencing reduced the growth of A549 cells. LncRNA BCYRN1 was involved in the metastasis of NSCLC through modulating the miR-30b-3p/ROCK1 axis.

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Section: Discussionsupporting

confidence: 55%

LncRNA BCYRN1 promotes cell migration and invasion of non-small cell lung cancer via the miR-30b-3p/ROCK1 axis

Song¹,

Wei-gang²,

Zhu³

et al. 2022

neo

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“…Our previous study [7] reported that F-actin and lamellipodium are vital for cancer mobilization. At the molecular level, F-actin multimerizes at the membrane and then forms the lamellipodium, which induces cellular deformation and migration [51]. In this study, immunofluorescence was used to observe alterations in the lamellipodium.…”

Section: F-actin/lamellipodium Signaling Pathway Is Impaired Bymentioning

confidence: 99%

Yap-Hippo Signaling Activates Mitochondrial Protection and Sustains Breast Cancer Viability under Hypoxic Stress

Chen

Zhang

Guo

et al. 2021

Journal of Oncology

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Yes-associated protein (Yap) is a transcriptional regulator that upregulates oncogenes and downregulates tumor repressor genes. In this study, we analyzed protein expression, RNA transcription, and signaling pathways to determine the function and mechanism of Yap in breast cancer survival during hypoxic stress. Yap transcription was drastically upregulated by hypoxia in a time-dependent manner. siRNA-mediated Yap knockdown attenuated breast cancer viability and impaired cell proliferation under hypoxic conditions. Yap knockdown induced mitochondrial stress, including mitochondrial membrane potential reduction, mitochondrial oxidative stress, and ATP exhaustion after exposure to hypoxia. It also repressed mitochondrial protective systems, including mitophagy and mitochondrial fusion upon exposure to hypoxia. Finally, our data showed that Yap knockdown suppresses MCF-7 cell migration by inhibiting F-actin transcription and promoting lamellipodium degradation under hypoxic stress. Taken together, Yap maintenance of mitochondrial function and activation of F-actin/lamellipodium signaling is required for breast cancer survival, migration, and proliferation under hypoxic stress.

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“…[17,18] Compared with normal cells, cancer cells have faster growth and invasive capabilities and require mitochondria to provide more energy. [19] Mitochondrial dysfunction is one of the signs of apoptosis induced by intrinsic pathway. [20] Mitochondria plays an important role in the regulation of apoptosis signals.…”

Section: Discussionmentioning

confidence: 99%

Oxaliplatin Induces Cell Cycle Arrest and Apoptosis in T-leukemia Cells through Mitochondrial and PI3K/Akt Signaling Pathways

Li¹,

Wang²,

Tian³

et al. 2021

Med. Res.

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Oxaliplatin (L-OHP) is a new platinum anticancer drug, which is used for the treatment of metastatic colorectal cancer or the adjuvant treatment of stage III colon cancer. T-cell acute lymphoblastic leukemias (T-ALLs) are invasive thymocytic malignant tumors with poor prognosis. The purpose of this study was to evaluate the cytotoxic effect of L-OHP on human T-ALL cell lines MOLT-4, Jurkat, CCRF-CEM, and CEM/C1 cells. The CCK-8 method results showed that L-OHP significantly inhibited T-ALL cells proliferation. The inhibition of these T-ALL cells prolife by L-OHP seems to be related to the induction of cell cycle arrest. The effect of L-OHP on the cell cycle distribution of T-ALL cells varies with cell types. As to cells apoptosis, Annexin V/Propidium iodide assay disclosed that L-OHP prominently induced T-ALL cells apoptosis by activating the pathways of mitochondrial biogenesis and is more sensitive to MOLT-4 cells. Western blot analysis showed that L-OHP treatment could promote apoptosis through down-regulated Bcl-2 protein level, up-regulated Bax and caspase-9 proteins levels and cell cycle arrest by inhibiting the PI3K/Akt signaling pathway in MOLT-4 cells. Our results indicate that L-OHP, as a new type of platinum anticancer drug, may attract more attention in the future treatment of T-ALL.

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<p>miR-31 Modulates Liver Cancer HepG2 Cell Apoptosis and Invasion via ROCK1/F-Actin Pathways</p>

Cited by 22 publications

References 52 publications

LncRNA BCYRN1 promotes cell migration and invasion of non-small cell lung cancer via the miR-30b-3p/ROCK1 axis

LncRNA BCYRN1 promotes cell migration and invasion of non-small cell lung cancer via the miR-30b-3p/ROCK1 axis

Yap-Hippo Signaling Activates Mitochondrial Protection and Sustains Breast Cancer Viability under Hypoxic Stress

Oxaliplatin Induces Cell Cycle Arrest and Apoptosis in T-leukemia Cells through Mitochondrial and PI3K/Akt Signaling Pathways

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