COL1A1, ITGB1, THY1, and PDGFRA: key immune-related genes in uterine corpus endometrial carcinoma with prognostic and therapeutic implications

Uterine corpus endometrial carcinoma (UCEC) is one of the most common gynecological malignancies, characterized by complex molecular alterations that drive its progression. Understanding the molecular mechanisms underlying UCEC is crucial for developing effective diagnostic, prognostic, and therapeutic strategies. Immune-related genes, such as COL1A1, ITGB1, THY1, and PDGFRA, have been implicated in various cancers, but their roles in UCEC remain underexplored. In this study, we investigate the roles of these genes in the development and progression of UCEC. Using both in silico and in vitro approaches, we found that these genes were dysregulated in UCEC. Our results revealed the downregulation of COL1A1, ITGB1, THY1, and PDGFRA in UCEC compared to normal tissues. Further, promoter methylation analysis showed increased methylation of these genes in UCEC. Survival analysis highlighted their potential as prognostic markers, with lower expression linked to poor patient survival. Additionally, genetic alteration analysis demonstrated mutations in these genes across UCEC patients. Our results also showed that overexpression of COL1A1 in KLE and HEC-1B cells significantly reduced cell proliferation, colony formation, and migration, indicating that COL1A1 overexpression impacts critical cellular behaviors in UCEC. Finally, we explored the therapeutic potential of targeting these genes, suggesting that they may offer valuable insights for personalized treatment strategies in UCEC. This study identifies COL1A1, ITGB1, THY1, and PDGFRA as crucial regulators of UCEC progression, with altered expression linked to tumor behavior and patient survival. Overexpression of COL1A1 impaired cell proliferation, colony formation, and migration. Future research should focus on elucidating the molecular mechanisms of these genes, exploring their therapeutic targeting in preclinical models, and validating their clinical potential as biomarkers in larger patient cohorts to improve treatment strategies for UCEC.

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Publication Details

Journal
Hereditas
Published
2025-08-15
DOI
https://doi.org/10.1186/s41065-025-00448-x
Citations
4
Primary Topic
Cancer-related molecular mechanisms research
Type
article
Field-Weighted Citation Impact
3.75

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article

COL1A1, ITGB1, THY1, and PDGFRA: key immune-related genes in uterine corpus endometrial carcinoma with prognostic and therapeutic implications

Taghreed N. Almanaa, Jehad S. Al‐Hawadi, Yasir Hameed, Ibrahim Saleh et al.
4 citations
Hereditas
Cancer-related molecular mechanisms research
3.75
article

COL1A1, ITGB1, THY1, and PDGFRA: key immune-related genes in uterine corpus endometrial carcinoma with prognostic and therapeutic implications

Taghreed N. Almanaa, Jehad S. Al‐Hawadi, Yasir Hameed, Ibrahim Saleh, Wahidah H. Al‐Qahtani, Mostafa A. Abdel-Maksoud, Abdulaziz Alamri, Naser Zomot
article en
4 citations

Abstract

Uterine corpus endometrial carcinoma (UCEC) is one of the most common gynecological malignancies, characterized by complex molecular alterations that drive its progression. Understanding the molecular mechanisms underlying UCEC is crucial for developing effective diagnostic, prognostic, and therapeutic strategies. Immune-related genes, such as COL1A1, ITGB1, THY1, and PDGFRA, have been implicated in various cancers, but their roles in UCEC remain underexplored. In this study, we investigate the roles of these genes in the development and progression of UCEC. Using both in silico and in vitro approaches, we found that these genes were dysregulated in UCEC. Our results revealed the downregulation of COL1A1, ITGB1, THY1, and PDGFRA in UCEC compared to normal tissues. Further, promoter methylation analysis showed increased methylation of these genes in UCEC. Survival analysis highlighted their potential as prognostic markers, with lower expression linked to poor patient survival. Additionally, genetic alteration analysis demonstrated mutations in these genes across UCEC patients. Our results also showed that overexpression of COL1A1 in KLE and HEC-1B cells significantly reduced cell proliferation, colony formation, and migration, indicating that COL1A1 overexpression impacts critical cellular behaviors in UCEC. Finally, we explored the therapeutic potential of targeting these genes, suggesting that they may offer valuable insights for personalized treatment strategies in UCEC. This study identifies COL1A1, ITGB1, THY1, and PDGFRA as crucial regulators of UCEC progression, with altered expression linked to tumor behavior and patient survival. Overexpression of COL1A1 impaired cell proliferation, colony formation, and migration. Future research should focus on elucidating the molecular mechanisms of these genes, exploring their therapeutic targeting in preclinical models, and validating their clinical potential as biomarkers in larger patient cohorts to improve treatment strategies for UCEC.

HereditasVol. 162(1)
Zarqa University (JO), King Saud University (SA)
King Saud University
No poverty
Openalex Percentile: Top 6%
Cancer-related molecular mechanisms research
3.75
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