CircTIMELESS regulates the proliferation and invasion of lung squamous cell carcinoma cells via the miR‐136‐5p/ROCK1 axis

Zhang, Wenjing; Shi, Jingjing; Chuan-hao, Cheng; Wang, Huaqi

doi:10.1002/jcp.29521

Cited by 16 publications

(16 citation statements)

References 29 publications

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“…TargetScan 7.2 predicted that miR-576-3p targeted ROCK1. It has been reported that ROCK1 is a downstream target of miR-136-5p and that the miR-136-5p/ROCK1 axis participates in the inflammatory response induced by cerebral ischemia/reperfusion injury, as well as in the proliferation and invasion of LSCC cells (16,17). The present study also confirmed this relationship using a dual-luciferase reporter assay.…”

Section: Discussionsupporting

confidence: 86%

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The miR‑136‑5p/ROCK1 axis suppresses invasion and migration, and enhances cisplatin sensitivity in head and neck cancer cells

et al. 2021

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Laryngeal squamous cell carcinoma (LSCC) and hypopharyngeal squamous cell carcinoma (HPSCC) are two types of head and neck cancers with high incidence rates and relatively poor prognoses. The aim of the present study was to determine the effects of microRNA (miR/miRNA)-136-5p and its downstream target, Rho-associated coiled-coil containing protein kinase 1 (ROCK1), on LSCC and HPSCC progression and cisplatin sensitivity. The miRNA and protein expression levels in head and neck cancer cell lines were evaluated using reverse transcription-quantitative PCR and western blotting, respectively. MTT, wound healing assays, transwell assays and flow cytometry analysis were performed to measure cell properties. The binding between miR-136-5p and ROCK1 was detected using a dual-luciferase reporter assay. Autophagy double-labeled adenoviral infection assays were used to assess cell autophagy. The results showed that miR-136-5p was expressed in LSCC and HPSCC cells. Functional experiments showed that the expression of miR-136-5p in LSCC and HPSCC cells was negatively correlated with cell viability, invasion and migration. Additionally, miR-136-5p overexpression inhibited epithelial-mesenchymal transition, whereas miR-136-5p knockdown had the opposite effect. Dual-luciferase reporter assays confirmed the targeting relationship between miR-136-5p and ROCK1. miR-136-5p overexpression increased the cisplatin sensitivity of LSCC and HPSCC cells by reducing cell viability, as well as promoting cell apoptosis and autophagy. miR-136-5p overexpression decreased the expression levels of its downstream target ROCK1 and attenuated activity of the Akt/mTOR signaling pathway in cisplatin-treated LSCC and HPSCC cells. Conversely, miR-136-5p knockdown increased ROCK1 levels and decreased cisplatin sensitivity of the LSCC and HPSCC cells by increasing cell viability and inhibiting cell apoptosis, which was reversed by ROCK1 inhibition using the ROCK1 inhibitor, Y27632. Taken together, the results showed that the miR-136-5p/ROCK1 axis inhibits cell invasion and migration, and increases the sensitivity of LSCC and HPSCC cells to cisplatin.

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Section: Discussionsupporting

confidence: 86%

“…A previous study reported the relationship between miR-136 and Rho-associated coiled-coil containing protein kinase (ROCK) 1 (16,17). ROCK1, one of the isoforms of the ROCK, is a downstream effector of Rho A and is activated when it selectively binds to GTP (18,19).…”

Section: Introductionmentioning

confidence: 99%

The miR‑136‑5p/ROCK1 axis suppresses invasion and migration, and enhances cisplatin sensitivity in head and neck cancer cells

et al. 2021

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“…The circTP63/FOXM1/miR-873-3p axis is identified to facilitate LUSC progression [ 10 ]. circTIMELESS regulates LUSC cell proliferation and invasion via the miR-136-5p/ROCK1 axis [ 11 ]. In this study, the ceRNA network of circCNN2/miR-184/E2F1 was identified in LUSC cells and related assays were carried out to testify its impact on LUSC progression.…”

Section: Introductionmentioning

confidence: 99%

circCNN2 Accelerates Cell Proliferation and Invasion in Lung Squamous Cell Carcinoma via Regulating miR-184/E2F1 and Activating MAPK Signaling Pathway

et al. 2022

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Circular RNAs (circRNAs) have been demonstrated as potential biomarkers for the diagnosis and treatment of human diseases. Previous studies have unveiled the carcinogenic role of circRNA_102399 (circCNN2) in lung cancer. Through the UALCAN database, it was found that CNN2, the parent gene of circCNN2, was specifically highly expressed in human lung squamous cell carcinoma (LUSC) cells, but the regulatory mechanism of circCNN2 in LUSC is unclear. In this study, circCNN2 expression in LUSC cells was examined via RT-qPCR, and its effects on LUSC progression was verified through functional assays. The subcellular localization of circCNN2 was identified via FISH assay, and the underlying mechanism of circCNN2 on the activation of MAPK signaling pathway was determined through mechanism experiments. Results demonstrated that circCNN2 was upregulated in LUSC cells, and it promoted LUSC cell proliferation and invasion. Besides, circCNN2 acted as a competing endogenous RNA (ceRNA) to sponge miR-184 to upregulate E2F transcription factor 1 (E2F1) expression. Furthermore, it was verified that circCNN2 activated the generic mitogen-activated protein kinases (MAPK) signaling pathway through E2F1 and thus promoting LUSC progression. In a word, this study indicated that circCNN2 activated MAPK signaling pathway through the miR-184/E2F1 axis to promote proliferation and invasion of LUSC cells.

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“…For example, miR-136-5p may inhibit HCC cell proliferation, migration and invasion by targeting the WNK1 pathway ( 32 ). It may also inhibit lung squamous cell carcinoma progression by deactivating ROCK1 ( 33 ). Furthermore, miR-136-5p has been reported to regulate the expression of IRX5 to suppress cell proliferation in HCC ( 34 ).…”

Section: Discussionmentioning

confidence: 99%

lncRNA MIR4435‑2HG promotes the progression of liver cancer by upregulating B3GNT5 expression

Zhu

et al. 2021

Mol Med Rep

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Several studies have indicated that dysregulation of long non-coding RNAs (lncRNAs) participates in the initiation and progression of cancer. The lncRNA MIR4435-2HG was previously reported to act as an oncogene in human cancer, including liver cancer. However, its role in the pathogenesis in liver cancer is largely unclear. The present study aimed to reveal the molecular mechanism by which MIR4435-2HG regulates liver cancer. The expression levels of MIR4435-2HG in liver cancer and adjacent normal tissues were analyzed using The Cancer Genome Atlas database. MIR4435-2HG expression was validated by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) in cancer cells in vitro . The target genes of MIR4435-2HG were predicted using bioinformatics analysis. Interactions between miR-136-5p, MIR4435-2HG and B3GNT5 were detected using luciferase reporter assays, and their effects on cell viability, migration and invasion were assessed using Cell Counting Kit-8, wound healing and Transwell assays. The effects of miR-136-5p and MIR4435-2HG on B3GNT5 expression were confirmed by western blot analysis. The results revealed that MIR4435-2HG expression was upregulated in primary liver cancer and liver cancer cell lines, and was positively associated with advanced tumor stage, metastasis and poor prognosis in patients with liver cancer. Knockdown of MIR4435-2HG significantly inhibited the proliferation, migration and invasion of liver cancer cells. Furthermore, miR-136-5p was determined to be a direct target of MIR4435-2HG and suppressed MIR4435-2HG expression by binding with the seed region of the 3′-UTR of MIR4435-2HG in liver cancer cells. Functional studies showed that the inhibitory effects of MIR4435-2HG knockdown on cell proliferation, migration and invasion were significantly rescued by inhibiting miR-136-5p. Furthermore, the target gene, B3GNT5, of miR-136-5p was confirmed by bioinformatics analysis and RT-qPCR. In addition, B3GNT5 expression was regulated by the MIR4435-2HG / miR-136-5p axis. In conclusion, the present study indicated that MIR4435-2HG facilitated the progression of liver cancer via the MIR4435-2HG / miR-136-5p / B3GNT5 axis, which demonstrated that MIR4435-2HG may be a potential biomarker for the prognosis and treatment of liver cancer.

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CircTIMELESS regulates the proliferation and invasion of lung squamous cell carcinoma cells via the miR‐136‐5p/ROCK1 axis

Cited by 16 publications

References 29 publications

The miR‑136‑5p/ROCK1 axis suppresses invasion and migration, and enhances cisplatin sensitivity in head and neck cancer cells

The miR‑136‑5p/ROCK1 axis suppresses invasion and migration, and enhances cisplatin sensitivity in head and neck cancer cells

circCNN2 Accelerates Cell Proliferation and Invasion in Lung Squamous Cell Carcinoma via Regulating miR-184/E2F1 and Activating MAPK Signaling Pathway

lncRNA MIR4435‑2HG promotes the progression of liver cancer by upregulating B3GNT5 expression

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