Amplified TPM1 suppresses non-small cell lung cancer cells proliferation and metastasis
Fengling Xu1, Jiangfeng Lv2, Shuang Qin2
1Blood Transfusion Department, Jinan City People's Hospital, People's Hospital Affiliated to Shandong First Medical University, Jinan, 271100, China.
Background:
TPM1 a member of TPM family and acts as a crucial role in a variety of tumors progression. However, the effect and mechanism of TPM1 on NSCLC need to be further explored. Here, effect and mechanism of TPM1 on NSCLC were revealed to provide new target for clinical therapy.
Methods:
TPM1 expression in NSCLC tissues and normal tissues was analyzed using GEPIA online database. NSCLC cells were transfected with TPM1 overexpression plasmid. TPM1 mRNA expression of NSCLC cells was assessed by RT-qPCR. NSCLC cells proliferation and apoptosis were detected by CCK-8 and flow cytometry. Scratch healing and Transwell experiments were introduced to measure NSCLC cells migration and invasion. The effects of TPM1 overexpression on TPM1, YAP1 and EMT related proteins expression in NSCLC cells were detected by Western blot experiments. The interaction between TPM1 and YAP1 was analyzed by the HitPredict database and Co-IP assay.
Results:
TPM1 expression in NSCLC was decreased. High expression of TPM1 could inhibit NSCLC cells proliferation, migration and invasion and promote apoptosis. EMT marker E-Cadherin increased in TPM1 overexpression group, while Vimentin and N-Cadherin decreased. EMT process was inhibited by TPM1 overexpression. There is a mutual binding between TPM1 and YAP1, and TPM1 could down-regulate YAP1 expression. Overexpressed YAP1 could partly counteract the inhibition of NSCLC cells proliferation and metastasis induced by TPM1 overexpression.
Conclusion:
TPM1 was down-regulated in NSCLC, and its overexpression inhibited NSCLC cells proliferation and metastasis, and this was achieved by regulating YAP1. TPM1 may become a new therapeutic target for NSCLC.
Insights
Tropomyosin 1 (TPM1) is downregulated in non-small cell lung cancer (NSCLC). Overexpressing TPM1 inhibits NSCLC cell proliferation and metastasis by regulating YAP1, offering a potential new therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
Background:
- Tropomyosin 1 (TPM1) plays a role in tumor progression.
- The specific role and mechanism of TPM1 in non-small cell lung cancer (NSCLC) require further investigation.
Purpose of the Study:
- To elucidate the effect and mechanism of TPM1 in NSCLC.
- To identify TPM1 as a potential therapeutic target for NSCLC.
Main Methods:
- TPM1 expression analysis in NSCLC tissues and normal tissues using GEPIA.
- Assessment of NSCLC cell proliferation, apoptosis, migration, and invasion following TPM1 overexpression.
- Western blot analysis of TPM1, YAP1, and EMT-related proteins.
- Co-immunoprecipitation (Co-IP) assay to confirm TPM1-YAP1 interaction.
Main Results:
- TPM1 expression is decreased in NSCLC.
- TPM1 overexpression inhibits NSCLC cell proliferation, migration, and invasion, while promoting apoptosis.
- TPM1 overexpression upregulates E-Cadherin and downregulates Vimentin and N-Cadherin, indicating inhibition of epithelial-mesenchymal transition (EMT).
- TPM1 binds to YAP1 and downregulates its expression; YAP1 overexpression partially reverses the inhibitory effects of TPM1.
Conclusions:
- TPM1 is downregulated in NSCLC.
- TPM1 overexpression inhibits NSCLC progression by regulating YAP1.
- TPM1 presents a promising therapeutic target for NSCLC treatment.
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