https://orcid.org/0000-0002-4330-072X
Abstract
Purpose
The extracellular matrix in the tumor microenvironment are closely related to the development of tumors. This study’s primary aim is to study the association between prolyl 3-hydroxylase 1 (P3H1) which mainly expresses collagen in extracellular matrix and the progression and prognosis of bladder cancer (BC).
Methods
The clinical and transcriptome data were acquired from the cancer genome atlas database. BLCAsubtyping is used to evaluate tissue subtypes of BC. The COX proportional hazards can be used to evaluate the survival process’s influencing factors. Immunohistochemistry was used to identify differences in the expression of P3H1 in cancer and paired adjacent tissues. GSEA was used to investigate the underlying biological processes. Finally, ssGSEA, TIMER and pRRophetic were used to study the relationship between P3H1 and immune cell infiltration and drug sensitivity.
Results
The expression of P3H1 was substantially higher in highly invasive BC samples than in low invasive BC. P3H1 was an independent predictor of overall survival (HR = 1.12, p = 0.03). P3H1 expression was significantly higher in tumor tissues than adjacent normal tissues in clinical tissue samples, and was significantly higher in highly stage cancer than low stage cancer samples. Samples with high P3H1 expression had a higher level of immune cell infiltration and immune function, as well as a significant correlation with macrophage and dendritic cell infiltration and TGF-beta, Th1 cells, and macrophage regulation (cor >0.3, p <0.05). P3H1 high expression samples were substantially more sensitive to docetaxel, cisplatin, vinblastine, camptothecin, paclitaxel, and other medicines than P3H1 low expression samples.
Discussion
P3H1 is a possible oncogene and an independent predictor of poor prognosis in BC; it also has enhanced sensitivity to docetaxel, cisplatin, vinblastine, camptothecin, paclitaxel, and other medications.
Data Accessibility
Publicly available datasets were analyzed in this study, these can be found in IMvigor210 cohort (http://research-pub.gene.com/IMvigor210CoreBiologies/packageVersions/), The Cancer GenomeAtlas (https://portal.gdc.cancer.gov).
Acknowledgments
This work was supported by the National Natural Science Foundation of China (grant No.82372685); Medical Science and Technology Research Fund Project of Guangdong Province of China (grant No. B2023489).
Author Contributions
All of the authors contributed significantly to the work that was published, whether it was through conception, study design, execution, data acquisition, analysis, and interpretation, or in all of these areas; they all contributed to draft, revise, or critically review the article; they approved the final version that was published; they all agreed on the journal to which the article was submitted; and they all agreed to take responsibility for the work in its entirety.
Disclosure
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.