Cysteine‐rich intestinal protein 1 enhances the progression of hepatocellular carcinoma via Ras signaling

Abstract The present study aimed to explore the expression and clinical significance of cysteine‐rich intestinal protein 1 (CRIP1) mRNA in the serum of patients with hepatocellular carcinoma (HCC). Reverse transcription polymerase chain reaction (RT‐PCR) was performed to explore the level of CRIP1 m...

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Main Authors: Hong‐Yu He, Li Hu
Format: Article
Language:English
Published: Wiley 2022-01-01
Series:Kaohsiung Journal of Medical Sciences
Subjects:
Online Access:https://doi.org/10.1002/kjm2.12445
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author Hong‐Yu He
Li Hu
author_facet Hong‐Yu He
Li Hu
author_sort Hong‐Yu He
collection DOAJ
description Abstract The present study aimed to explore the expression and clinical significance of cysteine‐rich intestinal protein 1 (CRIP1) mRNA in the serum of patients with hepatocellular carcinoma (HCC). Reverse transcription polymerase chain reaction (RT‐PCR) was performed to explore the level of CRIP1 mRNA in the tissues and serum of patients with HCC. Our data showed that the mRNA level of CRIP1 was significantly elevated in the serum and tissues of HCC patients. Moreover, serum CRIP1 mRNA was significantly elevated in HCC patients with larger tumor sizes and higher tumor node metastasis (TNM) stages. Receiver operating characteristic analysis showed that compared with a single marker, the combined detection of alpha‐fetoprotein, carcinoembryonic antigen, and CRIP1 had the highest accuracy, sensitivity, and specificity. Further study showed that the overexpression of CRIP1 enhanced the proliferation and migration of HepG2 cells, but the inhibition of CRIP1 decreased the proliferation and migration of HepG2 cells. Microarray assays and KyotoEncyclopedia of Genes and Genomes (KEGG) pathway analysis showed that overexpression of CRIP1 induced the activation of Ras signaling. Co‐immunoprecipitation (Co‐IP) assays indicated that CRIP1 could interact with Ras. To further evaluate whether CRIP1 interacts with Ras, a specific siRNA targeting Ras was selected. We found that Ras knockdown reduced the activation of Ras/AKT signaling even in HepG2 cells transfected with CRIP1. Moreover, elevated expression of CRIP1 increased the proliferation of HepG2 cells, but such effects could be abolished by silencing Ras. In summary, elevated CRIP1 levels enhanced the progression of CRIP1 via Ras signaling.
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spelling doaj-art-26d1f8d8ba944cffbcccba1c7fa4d2db2025-08-20T03:00:06ZengWileyKaohsiung Journal of Medical Sciences1607-551X2410-86502022-01-01381495810.1002/kjm2.12445Cysteine‐rich intestinal protein 1 enhances the progression of hepatocellular carcinoma via Ras signalingHong‐Yu He0Li Hu1Department of Ultrasound Tai'an Medical District, 960 Hospital of Chinese PLA Tai'an ChinaPhysical Examination Center, Tai'an Medical District, 960 Hospital of PLA Tai'an ChinaAbstract The present study aimed to explore the expression and clinical significance of cysteine‐rich intestinal protein 1 (CRIP1) mRNA in the serum of patients with hepatocellular carcinoma (HCC). Reverse transcription polymerase chain reaction (RT‐PCR) was performed to explore the level of CRIP1 mRNA in the tissues and serum of patients with HCC. Our data showed that the mRNA level of CRIP1 was significantly elevated in the serum and tissues of HCC patients. Moreover, serum CRIP1 mRNA was significantly elevated in HCC patients with larger tumor sizes and higher tumor node metastasis (TNM) stages. Receiver operating characteristic analysis showed that compared with a single marker, the combined detection of alpha‐fetoprotein, carcinoembryonic antigen, and CRIP1 had the highest accuracy, sensitivity, and specificity. Further study showed that the overexpression of CRIP1 enhanced the proliferation and migration of HepG2 cells, but the inhibition of CRIP1 decreased the proliferation and migration of HepG2 cells. Microarray assays and KyotoEncyclopedia of Genes and Genomes (KEGG) pathway analysis showed that overexpression of CRIP1 induced the activation of Ras signaling. Co‐immunoprecipitation (Co‐IP) assays indicated that CRIP1 could interact with Ras. To further evaluate whether CRIP1 interacts with Ras, a specific siRNA targeting Ras was selected. We found that Ras knockdown reduced the activation of Ras/AKT signaling even in HepG2 cells transfected with CRIP1. Moreover, elevated expression of CRIP1 increased the proliferation of HepG2 cells, but such effects could be abolished by silencing Ras. In summary, elevated CRIP1 levels enhanced the progression of CRIP1 via Ras signaling.https://doi.org/10.1002/kjm2.12445cysteine‐rich intestinal protein 1hepatocellular carcinomaRas signaling
spellingShingle Hong‐Yu He
Li Hu
Cysteine‐rich intestinal protein 1 enhances the progression of hepatocellular carcinoma via Ras signaling
Kaohsiung Journal of Medical Sciences
cysteine‐rich intestinal protein 1
hepatocellular carcinoma
Ras signaling
title Cysteine‐rich intestinal protein 1 enhances the progression of hepatocellular carcinoma via Ras signaling
title_full Cysteine‐rich intestinal protein 1 enhances the progression of hepatocellular carcinoma via Ras signaling
title_fullStr Cysteine‐rich intestinal protein 1 enhances the progression of hepatocellular carcinoma via Ras signaling
title_full_unstemmed Cysteine‐rich intestinal protein 1 enhances the progression of hepatocellular carcinoma via Ras signaling
title_short Cysteine‐rich intestinal protein 1 enhances the progression of hepatocellular carcinoma via Ras signaling
title_sort cysteine rich intestinal protein 1 enhances the progression of hepatocellular carcinoma via ras signaling
topic cysteine‐rich intestinal protein 1
hepatocellular carcinoma
Ras signaling
url https://doi.org/10.1002/kjm2.12445
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AT lihu cysteinerichintestinalprotein1enhancestheprogressionofhepatocellularcarcinomaviarassignaling