Evidence map›Paper›PMID 30899362›Full record

ArticleAmerican journal of translational research2019

CLIC1 promotes the progression of oral squamous cell carcinoma via integrins/ERK pathways.

Jiali Feng, Jie Xu, Ying Xu, Jun Xiong, Tingting Xiao, Chao Jiang, Xian Li, Qian Wang, Jie Li, Yong Li

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2019. 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
2.8field-weighted citation impact, top 9% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

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  11. CLIC1 knockout inhibits invasion and migration of gastric cancer by upregulating AMOT-p130 expression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
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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

10 authors at 1 institution in 1 country.

Jiali FengCollege of Stomatology, Chongqing Medical University Chongqing, China.
Jie XuCollege of Stomatology, Chongqing Medical University Chongqing, China.
Ying XuCollege of Stomatology, Chongqing Medical University Chongqing, China.
Jun XiongCollege of Stomatology, Chongqing Medical University Chongqing, China.
Tingting XiaoCollege of Stomatology, Chongqing Medical University Chongqing, China.
Chao JiangCollege of Stomatology, Chongqing Medical University Chongqing, China.
Xian LiCollege of Stomatology, Chongqing Medical University Chongqing, China.
Qian WangCollege of Stomatology, Chongqing Medical University Chongqing, China.
Jie LiCollege of Stomatology, Chongqing Medical University Chongqing, China.
Yong LiCollege of Stomatology, Chongqing Medical University Chongqing, China.
Chongqing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chloride intracellular channel 1 (CLIC1), a member of the chloride channel protein family, acts as a promoter in many malignancies, but its role in oral cancer remains unclear. Hence, this research aimed to explore the effects of CLIC1 on the progression of oral cancer cells in vitro, and we assessed its role in cell proliferation, apoptosis, migration, invasion, angiogenesis, and chemosensitivity to cisplatin and possible signaling pathways. The results demonstrated that CLIC1 depletion inhibited the proliferation, invasion, migration and angiogenesis of oral squamous cell carcinoma (OSCC) cells in vitro, but promoted cell apoptosis and increased the drug susceptibility to cisplatin. In contrast, CLIC1 upregulation was positively correlated with cell proliferation, invasion and migration and angiogenesis. Mechanistically, CLIC1 silencing decreased the levels of ITGαv, ITGβ1, p-ERK, vimentin, MMP2 and MMP9, and increased the levels of p-p38, E-cadherin, caspase3 and caspase9. CLIC1 overexpression enhanced the ITGαv, ITGβ1, p-ERK, vimentin, MMP2 and MMP9 levels and decreased E-cadherin expression. Overall, these results indicated that CLIC1 promotes the progression of OSCC, and we speculated that its potential mechanism may be related to the regulation of ITGαv and ITGβ1, which led to activation of the MAPK/ERK and MAPK/p38 signal pathways.

Indexed as

apoptosisCLIC1IntegrinmigrationOSCCpathways

Identifiers

PMID30899362
PMCPMC6413291
OpenAlexW2989648556

What OpenQuestion holds

Textmetadata
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.