COMPREHENSIVE ANALYSIS OF COL1A1 EXPRESSION, METHYLATION, AND GENETIC ALTERATIONS IN LIVER HEPATOCELLULAR CARCINOMA

Main Article Content

Zainab lanjar
Rohma Fatima
Maryam Saddiqa
Muhammad Khizer Hayat
Imtiaz Ali Soomro
Tayyaba Riaz
Umair Younas
Qaiser Akram
Muhammad Ahsan Naeem
Muhammad Adnan Aslam
Rizwana Sultan

Keywords

LIHC, COL1A1, Diagnosis, Treatment

Abstract

Liver hepatocellular carcinoma (LIHC) is a prevalent and deadly form of liver cancer characterized by significant genetic and epigenetic alterations. This study focuses on the role of COL1A1, a gene implicated in various cancers, by analyzing its expression, promoter methylation, and genetic mutations in LIHC. Using the UALCAN database, we observed a significant upregulation of COL1A1 in LIHC samples compared to normal controls, suggesting its involvement in cancer progression. This finding was corroborated by GEPIA2 analysis, which also showed elevated COL1A1 expression in LIHC. Further analysis using UALCAN revealed that COL1A1 expression was consistently upregulated across different cancer stages, races, ages, and genders of LIHC patients, indicating its broad role in tumor development. Validation with GEPIA2 confirmed these observations at individual cancer stages. Methylation analysis showed that COL1A1 was hypomethylated in LIHC samples relative to normal controls, a factor known to enhance tumor development. Interestingly, stage-specific analysis indicated hypermethylation of COL1A1 in stage 4 LIHC, reflecting its complex regulatory mechanisms. Survival analysis using KM plotter and GEPIA2 indicated that higher COL1A1 expression was associated with lower overall survival (OS) rates in LIHC patients, although the results were not statistically significant. Genetic alteration analysis via cBioPortal identified a low mutation frequency (3%) in COL1A1, suggesting limited impact on LIHC through genetic mutations alone. In conclusion, our comprehensive analysis highlights COL1A1 as a potentially significant player in LIHC progression through its aberrant expression and methylation, although its direct genetic mutations appear to have minimal effect. These findings underscore the need for further research to fully elucidate COL1A1's role and therapeutic potential in LIHC.

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