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The prognostic value of TPM1–4 in hepatocellular carcinoma

BACKGROUND: Despite advances in multiple disciplinary diagnoses and treatments, the prognosis of hepatocellular carcinoma (HCC) remains poor. Some evidence has identified that the aberrant expression of tropomyosins (TPMs) is involved with some cancers development. However, prognostic values of TPMs...

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Detalles Bibliográficos
Autores principales: Tian, Zhihui, Zhao, Jian, Wang, Yusheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8729055/
https://www.ncbi.nlm.nih.gov/pubmed/34850589
http://dx.doi.org/10.1002/cam4.4453
Descripción
Sumario:BACKGROUND: Despite advances in multiple disciplinary diagnoses and treatments, the prognosis of hepatocellular carcinoma (HCC) remains poor. Some evidence has identified that the aberrant expression of tropomyosins (TPMs) is involved with some cancers development. However, prognostic values of TPMs in HCC have not been thoroughly investigated. METHODS: Original TPM1–4 mRNA expression of TCGA HCC data and GTEx was downloaded from UCSC XENA. Oncomine database and GSE46408 were used for verification. Clinical stages and survival analysis of TPM1–4 in HCC were performed by GEPIA2. cBioPortal was utilized to assess TPM1–4 gene alteration in HCC. TIMER2.0 was used for investigating the relevance of TPM1–4 to tumor‐infiltrating immune cells in HCC. Additionally, we constructed a TPM1–4 prognostic model to explore the value of TPM1–4 for prognostic evaluation in HCC. LinkedOmics was applied to elucidate TPM3 co‐expression networks in HCC. RESULTS: This present study showed that TPM1–4 was upregulated in all HCC tissues, and TPM3 overexpression was correlated with poor survival outcomes in patients with HCC. Besides, TPM3 amplification was the main altered type in TPM1–4 genetic alteration, which affected the prognosis of HCC patients. The risk model revealed that TPM1, TPM2, and TPM3 were applied to risk assessment of HCC prognosis, among which TPM3 expression was significantly higher in the high‐risk group than that in the low‐risk group. Univariate and multivariate cox regression analyses indicated that TPM3 may be an independent prognostic factor of HCC prognosis. In addition, TPM3 co‐expression genes mainly participated in the cell cycle by maintaining microtubule cytoskeleton in HCC progression. TPM1–4 was associated with some tumor‐infiltrating immune cells in HCC. CONCLUSION: Our study detected that the expression level of TPM1–4 was all remarkably elevated in HCC, suggesting that TPM1–4 may serve an important role in HCC development. High TPM3 expression was found to be correlated with poor overall survival, and TPM3 may be an independent prognostic factor for HCC.