Evidence map›Paper›PMID 34715922›Full record

ArticleCell & bioscience2021

PRCC reduces the sensitivity of cancer cells to DNA damage by inhibiting JNK and ATM/ATR pathways and results in a poor prognosis in hepatocellular carcinoma.

Chunying Liu, Xuejing Lin, Bin Sun, Ziming Mao, Lei Chen, Haihua Qian, Changqing Su

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 39% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Chunying Liu *Department of Molecular Oncology, Eastern Hepatobiliary Surgery Hospital, Navy Military Medical University, Shanghai, 200438, People's Republic of China.
Xuejing Lin *Department of Molecular Oncology, Eastern Hepatobiliary Surgery Hospital, Navy Military Medical University, Shanghai, 200438, People's Republic of China.
Bin Sun *Department of Molecular Oncology, Eastern Hepatobiliary Surgery Hospital, Navy Military Medical University, Shanghai, 200438, People's Republic of China.
Ziming MaoDepartment of Molecular Oncology, Eastern Hepatobiliary Surgery Hospital, Navy Military Medical University, Shanghai, 200438, People's Republic of China.
Lei ChenDepartment of Molecular Oncology, Eastern Hepatobiliary Surgery Hospital, Navy Military Medical University, Shanghai, 200438, People's Republic of China.
Haihua QianDepartment of Molecular Oncology, Eastern Hepatobiliary Surgery Hospital, Navy Military Medical University, Shanghai, 200438, People's Republic of China.
Changqing SuDepartment of Molecular Oncology, Eastern Hepatobiliary Surgery Hospital, Navy Military Medical University, Shanghai, 200438, People's Republic of China. suchangqing@gmail.com.
Second Military Medical University · CNEastern Hepatobiliary Surgery Hospital · CN

Funding

National Key R&D Program of China 2018YFA0900902National Natural Science Foundation of China 81702735National Natural Science Foundation of China 81773251
6 · The paper itself

Abstract

BACKGROUND AND

aimThe proline rich mitotic checkpoint control factor (PRCC) is involved in the splicing process of pre-mRNA. This study aims to elucidate PRCC molecular function, regulatory mechanism and diagnostic value in hepatocellular carcinoma (HCC).

methodsThe tissue microarray and serum samples from HCC patients were used to investigate the clinical value of PRCC. The biological function and molecular mechanism of PRCC were demonstrated by cell biology, biochemical and animal experiments. The relationship between PRCC and intratumoral heterogeneity (ITH) was analyzed by bioinformatics.

resultsPRCC was highly expressed in HCC tissues and related to the poor prognosis of HCC patients, its contents were elevated in the preoperative sera of HCC patients. PRCC exhibited high application potential as a substitute or adjuvant of alpha-fetoprotein (AFP) for clinical diagnosis of HCC. It had no significant effect on the proliferation of cancer cells, but could inhibit spheroid formation and metastasis of HCC cells in vitro and in vivo. The high ectopic expression of PRCC made cancer cells insensitive to DNA damage, and enhanced the heterogeneity of HCC cells by inhibiting the JNK/ATM/ATR/ATF2 axis. The HCC patients with high PRCC expression had high ITH, which corresponded to a short overall survival in patients.

conclusionsPRCC has high application potential as a substitute or adjuvant of AFP for clinical diagnosis of HCC. The high ectopic expression of PRCC not only caused HCC cells to resist to cell death induced by DNA damage, but also endowed cancer cells with numerous DNA mutations to become increasingly heterogeneous, finally leading to a poor prognosis in HCC patients. These data suggested PRCC could be a promising therapeutic target in HCC patients.

Indexed as

DNA damageHepatocellular carcinomaJNK signaling pathwayPRCCPrognosis

Identifiers

PMID34715922
PMCPMC8555229
OpenAlexW3208094193

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.