TY - JOUR
T1 - PRKRIP1, A Splicing Complex Factor, Is a Marker of Poor Prognosis in Colorectal Cancer
AU - Ozato, Yuki
AU - Masuda, Takaaki
AU - Kobayashi, Yuta
AU - Takao, Seiichiro
AU - Hisamatu, Yuuichi
AU - Toshima, Takeo
AU - Yonemura, Yusuke
AU - Uemura, Mamoru
AU - Eguchi, Hidetoshi
AU - Doki, Yuichiro
AU - Mori, Masaki
AU - Mimori, Koshi
N1 - Funding Information:
This study was funded by the Oita Cancer Research Foundation (grant number: JP20cm0106475h0001), Takeda Science Foundation, Japan Agency for Medical Research and Development (grant number: JP20cm0106475h0001), and the Japan Society for the Promotion of Science (grant numbers: 19H03715, 19K09176, 20H05039, 20K08930).
Publisher Copyright:
© 2022 International Institute of Anticancer Research. All rights reserved.
PY - 2022/10
Y1 - 2022/10
N2 - Background/Aim: Alternative splicing plays a vital role in cancer development and progression. The splicing C complex is involved in alternative splicing. However, the role of PRKR-interacting protein 1 (PRKRIP1), a component of the splicing C complex, in colorectal cancer (CRC) remains unclear. This study aimed to determine the clinicopathological, biological and prognostic significance of PRKRIP1 expression in CRC. Materials and Methods: We used a bioinformatics approach to screen for oncogenes using The Cancer Genome Atlas (TCGA) and Cancer Cell Line Encyclopedia (CCLE) datasets and identified PRKRIP1 as a driver gene on chromosome 7q. The mRNA expression of PRKRIP1 was measured using reverse transcription-quantitative PCR in 165 surgically resected CRC samples in our hospital, and its localization was determined using immunohistochemical staining. Gene Set Enrichment Analysis (GSEA) was performed using TCGA dataset. Results: High PRKRIP1 expression was significantly associated with poor prognosis in both the samples and TCGA dataset. A positive correlation was observed between copy number variation and PRKRIP1 expression in TCGA and CCLE datasets, and the frequency of PRKRIP1 mutations was less than 5%. Immunohistochemistry revealed that PRKRIP1 was located in the cytoplasm of tumor cells. GSEA revealed that PRKRIP1 expression was correlated with apoptosis-related gene sets. Conclusion: PRKRIP1 overexpression may be a poor prognostic biomarker for CRC. Although it is known that PRKRIP1, a spliceosome factor, is essential for splicing, we now revealed the way by which its expression accelerates CRC progression.
AB - Background/Aim: Alternative splicing plays a vital role in cancer development and progression. The splicing C complex is involved in alternative splicing. However, the role of PRKR-interacting protein 1 (PRKRIP1), a component of the splicing C complex, in colorectal cancer (CRC) remains unclear. This study aimed to determine the clinicopathological, biological and prognostic significance of PRKRIP1 expression in CRC. Materials and Methods: We used a bioinformatics approach to screen for oncogenes using The Cancer Genome Atlas (TCGA) and Cancer Cell Line Encyclopedia (CCLE) datasets and identified PRKRIP1 as a driver gene on chromosome 7q. The mRNA expression of PRKRIP1 was measured using reverse transcription-quantitative PCR in 165 surgically resected CRC samples in our hospital, and its localization was determined using immunohistochemical staining. Gene Set Enrichment Analysis (GSEA) was performed using TCGA dataset. Results: High PRKRIP1 expression was significantly associated with poor prognosis in both the samples and TCGA dataset. A positive correlation was observed between copy number variation and PRKRIP1 expression in TCGA and CCLE datasets, and the frequency of PRKRIP1 mutations was less than 5%. Immunohistochemistry revealed that PRKRIP1 was located in the cytoplasm of tumor cells. GSEA revealed that PRKRIP1 expression was correlated with apoptosis-related gene sets. Conclusion: PRKRIP1 overexpression may be a poor prognostic biomarker for CRC. Although it is known that PRKRIP1, a spliceosome factor, is essential for splicing, we now revealed the way by which its expression accelerates CRC progression.
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U2 - 10.21873/anticanres.15974
DO - 10.21873/anticanres.15974
M3 - Article
C2 - 36192001
AN - SCOPUS:85139103181
SN - 0250-7005
VL - 42
SP - 4701
EP - 4706
JO - Anticancer research
JF - Anticancer research
IS - 10
ER -