Evidence map›Paper›PMID 34585826›Full record

ArticleThe Kaohsiung journal of medical sciences2022

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

Hong-Yu He, Li Hu

Abstract read
In one paragraph

Article in The Kaohsiung journal of medical sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

2 authors.

Hong-Yu HeDepartment of Ultrasound, Tai'an Medical District, 960 Hospital of Chinese PLA, Tai'an, China.
Li HuPhysical Examination Center, Tai'an Medical District, 960 Hospital of PLA, Tai'an, China.ORCID https://orcid.org/0000-0001-5551-0962

Funding

960 Hospital of Chinese PLA PLA-201225
6 · The paper itself

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.

Indexed as

Signal Transductionalpha-FetoproteinsCarcinoembryonic AntigenCarcinoma, HepatocellularCarrier ProteinsCell MovementCell ProliferationCysteineHep G2 CellsHumansLIM Domain ProteinsLiver NeoplasmsRNA, MessengerRNA, Small Interferingalpha-FetoproteinsCarcinoembryonic AntigenCarrier ProteinsCRIP1 protein, humanCysteineLIM Domain ProteinsRNA, MessengerRNA, Small Interferingcysteine-rich intestinal protein 1hepatocellular carcinomaRas signaling

Identifiers

PMID34585826
PMCPMC11896244

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.