Evidence map›Paper›PMID 32905514›Full record

ArticleAmerican journal of cancer research2020

Up-regulation of CLIC1 activates MYC signaling and forms a positive feedback regulatory loop with MYC in Hepatocellular carcinoma.

Xiang Jiang, Yingyi Liu, Ganggang Wang, Ye Yao, Chengjie Mei, Xiaoling Wu, Weijie Ma, Yufeng Yuan

Abstract read
In one paragraph

Article in American journal of cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Chloride intracellular channels in oncology as potential novel biomarkers and personalized therapy targets: a systematic review.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2024
    Review
  5. Article
  6. Intracellular chloride channel 1 and tumor.American journal of cancer research · 2023
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. 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

8 authors.

Xiang JiangDepartment of Hepatobiliary and Pancreatic Surgery, Zhongnan Hospital of Wuhan University Wuhan 430071, Hubei, PR China.
Yingyi LiuDepartment of Hepatobiliary and Pancreatic Surgery, Zhongnan Hospital of Wuhan University Wuhan 430071, Hubei, PR China.
Ganggang WangDepartment of Hepatobiliary and Pancreatic Surgery, Zhongnan Hospital of Wuhan University Wuhan 430071, Hubei, PR China.
Ye YaoDepartment of Hepatobiliary and Pancreatic Surgery, Zhongnan Hospital of Wuhan University Wuhan 430071, Hubei, PR China.
Chengjie MeiDepartment of Hepatobiliary and Pancreatic Surgery, Zhongnan Hospital of Wuhan University Wuhan 430071, Hubei, PR China.
Xiaoling WuDepartment of Hepatobiliary and Pancreatic Surgery, Zhongnan Hospital of Wuhan University Wuhan 430071, Hubei, PR China.
Weijie MaDepartment of Hepatobiliary and Pancreatic Surgery, Zhongnan Hospital of Wuhan University Wuhan 430071, Hubei, PR China.
Yufeng YuanDepartment of Hepatobiliary and Pancreatic Surgery, Zhongnan Hospital of Wuhan University Wuhan 430071, Hubei, PR China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is leading cause of tumor-related deaths worldwide. The intracellular chloride channel protein (CLIC1) plays a role in the occurrence and progression of HCC, although the underlying mechanisms are still unclear. We evaluated the CLIC1 mRNA and protein levels in both patient tissues and HCC cell lines, and analyzed the correlation between CLIC1 expression and clinical features. The biological function of CLIC1 in HCC was examined in vivo and in vitro. The upstream regulatory factors were identified by bioinformatics programs, and downstream mechanisms affecting HCC behavior have also been explored and validated. CLIC1 was up-regulated in HCC tissues and cell lines, and promoted the proliferation, invasion and migration of HCC cells in vivo and in vitro. TP53 was identified as the upstream transcription factor of CLIC1. MiR-122-5p also regulated CLIC1 levels by degrading the transcripts. More importantly, we found that the increased CLIC1 was significantly related to the activation of MYC signaling. By binding with MYC, CLIC1 enhanced the transcription activity of MYC to downstream genes, rather than by altering its expression. Finally, a positive feedback regulatory loop between CLIC1 and MYC was established. CLIC1 is closely related to the occurrence, progression and prognosis of HCC, and a promising novel therapeutic target.

Indexed as

CLIC1Hepatocellular carcinomamiR-122-5pMYCTP53

Identifiers

PMID32905514
PMCPMC7471371

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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.