Dataset Information

Overexpression of mir-489-3p inhibits proliferation and migration of non-small cell lung cancer cells by suppressing the HER2/PI3K/AKT/Snail signaling pathway.

ABSTRACT:

Background

Lung cancer is a highly prevalent malignancy with significant morbidity and mortality rates. MiR-489-3p, a microRNA, has been identified as a regulator of tumor cell proliferation and invasion. Its expression is downregulated in non-small cell lung cancer (NSCLC). Elucidating the molecular mechanisms underlying miR-489-3p's role in NSCLC pathogenesis is crucial for identifying potential diagnostic and therapeutic targets.

Methods

To investigate the molecular mechanism of miR-489-3p in NSCLC, this study utilized A549, a commonly used NSCLC cell line. MiR-489-3p mimics and inhibitors were transfected into A549 cells. Additionally, co-transfection experiments using wortmannin, an inhibitor of the PI3K/AKT pathway, were performed. Expression of miR-489-3p and related proteins was analyzed by Western blotting and quantitative real-time PCR (qRT-PCR). Cell migration and proliferation were assessed by wound healing and colony formation assays, respectively.

Results

Overexpression of miR-489-3p significantly inhibited the proliferation and migration of A549 cells. This inhibitory effect was further enhanced upon co-transfected with wortmannin. Analysis of human lung specimens showed increased expression of HER2, PI3K, and AKT in lung adenocarcinoma tissues compared to adjacent non-cancerous tissues.

Conclusions

These findings suggest that miR-489-3p overexpression may inhibit NSCLC cell proliferation and migration by suppressing the HER2/PI3K/AKT/Snail signaling pathway. This study elucidates miR-489-3p's molecular mechanisms in NSCLC and provides experimental basis for identifying early diagnostic markers and novel therapeutic targets.

SUBMITTER: Cheng D

PROVIDER: S-EPMC11367056 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature

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Publications

Overexpression of mir-489-3p inhibits proliferation and migration of non-small cell lung cancer cells by suppressing the HER2/PI3K/AKT/Snail signaling pathway.

Cheng Di D Liu Zhong Z Sun Renren R Jiang Yun Y Zeng Zhaoming Z Zhao Rui R Mo Zhongcheng Z

Heliyon 20240806 16

<h4>Background</h4>Lung cancer is a highly prevalent malignancy with significant morbidity and mortality rates. MiR-489-3p, a microRNA, has been identified as a regulator of tumor cell proliferation and invasion. Its expression is downregulated in non-small cell lung cancer (NSCLC). Elucidating the molecular mechanisms underlying miR-489-3p's role in NSCLC pathogenesis is crucial for identifying potential diagnostic and therapeutic targets.<h4>Methods</h4>To investigate the molecular mechanism o ...[more]

PMID: 39224367

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Project description:We previously reported that relative to normal cervical mucus, microRNA 126‑3p (miR‑126‑3p) is present in significantly greater amounts in the cervical mucus of patients with overt cervical cancer or precursor lesions. Here, we investigated the effects of enforced miR‑126‑3p expression in the cervical cancer cell line, HeLa, on proliferation, migration, invasion, apoptosis and protein expression. We transfected HeLa cells with miR‑126‑3p miRNA and found that proliferation, migration and invasion by cell counting, wound healing, cell migration and invasion assay were significantly reduced in these cells relative to those transfected with a negative control mimic. The levels of phosphoinositide 3 kinase (PI3K), phosphorylated 3‑phosphoinositide‑dependent protein kinase‑1 (p‑PDK1) and p‑AKT proteins were lower in the miR‑126‑3p‑transfected cells. Phosphorylated 70S6K (p‑p70S6K), phosphorylated glycogen synthase kinase 3β (p‑GSK3β), phosphorylated S6K (p‑S6K), cyclin D1, phosphorylated p21‑activated kinase 1 (p‑PAK1), Rho associated coiled‑coil containing protein kinase 1 (ROCK1), myotonic dystrophy‑related CDC42‑binding kinases α (MRCKα) and phospholipase C γ1 (p‑PLCγ1) were also downregulated. This suggests that downstream effectors of the PI3K/PDK1/AKT pathway are targets for inhibition by miR‑126‑3p. In contrast, apoptotic‑related proteins including the BCL‑2‑associated agonist of cell death (Bad), B‑cell lymphoma‑extra‑large (Bcl‑xL) and BCL‑2‑associated X (Bax), were all upregulated by miR‑126‑3p, resulting in increased caspase 3/7 activity and apoptosis. Thus, enforced expression of miR‑126‑3p inhibited cell migration and invasion and also induced apoptosis by regulating the PI3K/PDK1/AKT pathway in HeLa cells. Hence, high levels of miR‑126‑3p may inhibit cervical carcinogenesis, and targeting the PI3K/PDK1/AKT pathway via miR‑126‑3p could represent a new approach for treating patients with cervical cancer.

Dataset Information

Overexpression of mir-489-3p inhibits proliferation and migration of non-small cell lung cancer cells by suppressing the HER2/PI3K/AKT/Snail signaling pathway.

Background

Methods

Results

Conclusions

Publications

Overexpression of mir-489-3p inhibits proliferation and migration of non-small cell lung cancer cells by suppressing the HER2/PI3K/AKT/Snail signaling pathway.

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