CTHRC1 expression is a novel shared diagnostic and prognostic biomarker of survival in six different human cancer subtypes
Abstract According to the previous reports, the collagen triple helix repeat containing 1 (CTHRC1) causes tumorigenesis by modulating the tumor microenvironment, however, the evidence is limited to a few human cancer subtypes. In the current study, we analyzed and validated the CTHRC1 expression var...
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2021
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oai:doaj.org-article:4ed568724e8a4fb0a3ea27a498ac32892021-12-02T18:01:41ZCTHRC1 expression is a novel shared diagnostic and prognostic biomarker of survival in six different human cancer subtypes10.1038/s41598-021-99321-w2045-2322https://doaj.org/article/4ed568724e8a4fb0a3ea27a498ac32892021-10-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-99321-whttps://doaj.org/toc/2045-2322Abstract According to the previous reports, the collagen triple helix repeat containing 1 (CTHRC1) causes tumorigenesis by modulating the tumor microenvironment, however, the evidence is limited to a few human cancer subtypes. In the current study, we analyzed and validated the CTHRC1 expression variations in 24 different human cancer tissues paired with normal tissues using publically available databases. We observed that CTHRC1 was overexpressed in all the 24 major subtypes of human cancers and its overexpression was significantly associated with the reduced overall survival (OS) duration of head and neck squamous cell carcinoma (HNSC), kidney renal clear cell carcinoma (KIRC), liver hepatocellular carcinoma (LIHC), Lung adenocarcinoma (LUAD), stomach adenocarcinoma (STAD), and Uterine corpus endometrial carcinoma (UCEC). This implies that CTHRC1 plays a significant role in the development and progression of these cancers. We further noticed that CTHRC1 was also overexpressed in HNSC, KIRC, LIHC, LUAD, STAD, and UCEC patients of different clinicopathological features. Pathways enrichment analysis revealed the involvement of CTHRC1 associated genes in seven diverse pathways. We also explored few interesting correlations between CTHRC1 expression and promoter methylation, genetic alterations, CNVs, CD8+ T immune cells infiltration, and tumor purity. In conclusion, CTHRC1 can serve as a shared diagnostic and prognostic biomarker in HNSC, KIRC, LIHC, LUAD, STAD, and UCEC patients of different clinicopathological features.Nuzhat SialMukhtiar AhmadMuhammad Safdar HussainMuhammad Junaid IqbalYasir HameedMehran KhanMustansar AbbasRizwan AsifJalil Ur RehmanMuhammad AtifMuhammad Rashid KhanZahid HameedHina SaeedRida TanveerSaba SaeedAneeqa SharifHafiz Muhammad AsifNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-18 (2021) |
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Medicine R Science Q Nuzhat Sial Mukhtiar Ahmad Muhammad Safdar Hussain Muhammad Junaid Iqbal Yasir Hameed Mehran Khan Mustansar Abbas Rizwan Asif Jalil Ur Rehman Muhammad Atif Muhammad Rashid Khan Zahid Hameed Hina Saeed Rida Tanveer Saba Saeed Aneeqa Sharif Hafiz Muhammad Asif CTHRC1 expression is a novel shared diagnostic and prognostic biomarker of survival in six different human cancer subtypes |
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Abstract According to the previous reports, the collagen triple helix repeat containing 1 (CTHRC1) causes tumorigenesis by modulating the tumor microenvironment, however, the evidence is limited to a few human cancer subtypes. In the current study, we analyzed and validated the CTHRC1 expression variations in 24 different human cancer tissues paired with normal tissues using publically available databases. We observed that CTHRC1 was overexpressed in all the 24 major subtypes of human cancers and its overexpression was significantly associated with the reduced overall survival (OS) duration of head and neck squamous cell carcinoma (HNSC), kidney renal clear cell carcinoma (KIRC), liver hepatocellular carcinoma (LIHC), Lung adenocarcinoma (LUAD), stomach adenocarcinoma (STAD), and Uterine corpus endometrial carcinoma (UCEC). This implies that CTHRC1 plays a significant role in the development and progression of these cancers. We further noticed that CTHRC1 was also overexpressed in HNSC, KIRC, LIHC, LUAD, STAD, and UCEC patients of different clinicopathological features. Pathways enrichment analysis revealed the involvement of CTHRC1 associated genes in seven diverse pathways. We also explored few interesting correlations between CTHRC1 expression and promoter methylation, genetic alterations, CNVs, CD8+ T immune cells infiltration, and tumor purity. In conclusion, CTHRC1 can serve as a shared diagnostic and prognostic biomarker in HNSC, KIRC, LIHC, LUAD, STAD, and UCEC patients of different clinicopathological features. |
format |
article |
author |
Nuzhat Sial Mukhtiar Ahmad Muhammad Safdar Hussain Muhammad Junaid Iqbal Yasir Hameed Mehran Khan Mustansar Abbas Rizwan Asif Jalil Ur Rehman Muhammad Atif Muhammad Rashid Khan Zahid Hameed Hina Saeed Rida Tanveer Saba Saeed Aneeqa Sharif Hafiz Muhammad Asif |
author_facet |
Nuzhat Sial Mukhtiar Ahmad Muhammad Safdar Hussain Muhammad Junaid Iqbal Yasir Hameed Mehran Khan Mustansar Abbas Rizwan Asif Jalil Ur Rehman Muhammad Atif Muhammad Rashid Khan Zahid Hameed Hina Saeed Rida Tanveer Saba Saeed Aneeqa Sharif Hafiz Muhammad Asif |
author_sort |
Nuzhat Sial |
title |
CTHRC1 expression is a novel shared diagnostic and prognostic biomarker of survival in six different human cancer subtypes |
title_short |
CTHRC1 expression is a novel shared diagnostic and prognostic biomarker of survival in six different human cancer subtypes |
title_full |
CTHRC1 expression is a novel shared diagnostic and prognostic biomarker of survival in six different human cancer subtypes |
title_fullStr |
CTHRC1 expression is a novel shared diagnostic and prognostic biomarker of survival in six different human cancer subtypes |
title_full_unstemmed |
CTHRC1 expression is a novel shared diagnostic and prognostic biomarker of survival in six different human cancer subtypes |
title_sort |
cthrc1 expression is a novel shared diagnostic and prognostic biomarker of survival in six different human cancer subtypes |
publisher |
Nature Portfolio |
publishDate |
2021 |
url |
https://doaj.org/article/4ed568724e8a4fb0a3ea27a498ac3289 |
work_keys_str_mv |
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