Evidence map›Paper›PMID 31164625›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2019

Calcium-Activated Chloride Channel A4 (CLCA4) Plays Inhibitory Roles in Invasion and Migration Through Suppressing Epithelial-Mesenchymal Transition via PI3K/AKT Signaling in Colorectal Cancer.

Hua Chen, Yang Liu, Cai-Jian Jiang, Yan-Min Chen, Hong Li, Qin-An Liu

Open access · greenAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

29 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Calcium channels as pharmacological targets for cancer therapy.Clinical and experimental medicine · 2025
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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

6 authors at 1 institution in 1 country.

Hua ChenDepartment of General Surgery, The First People's Hospital of Changde, Changde, Hunan, China (mainland).
Yang LiuDepartment of General Surgery, The First People's Hospital of Changde, Changde, Hunan, China (mainland).
Cai-Jian JiangDepartment of General Surgery, The First People's Hospital of Changde, Changde, Hunan, China (mainland).
Yan-Min ChenDepartment of General Surgery, The First People's Hospital of Changde, Changde, Hunan, China (mainland).
Hong LiDepartment of General Surgery, The First People's Hospital of Changde, Changde, Hunan, China (mainland).
Qin-An LiuDepartment of General Surgery, The First People's Hospital of Changde, Changde, Hunan, China (mainland).
The First People's Hospital of Changde · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Calcium-activated chloride channel A4 (CLCA4) is known as a tumor suppressor which contributes to the progression of a number of types of malignant tumors. However, little is known about the functional roles of CLCA4 in colorectal cancer (CRC). MATERIAL AND METHODS In this study, the expression patterns and dysregulation of mRNAs in CRC tissues were profiled by analyzing GSE21510 datasets from Gene Expression Omnibus database which contains 104 primary hepatocellular carcinoma tissues and 24 normal liver tissues, and by performing Kaplan-Meier analysis of TCGA data. Additionally, immunohistochemistry and quantitative real-time polymerase chain reaction (qRT-PCR) were performed using clinical tissues collected at our institute. In order to explore the functional role of CLCA4, gain-of-function cell models were constructed in SW620 and LoVo cells. Wound healing assay and Transwell assay were carried out to access the cell migration and invasion ability. RESULTS It was found that CLCA4 was an independent predictor for overall survival and lymph node metastasis. Additionally, immunohistochemistry and qRT-PCR results of the clinical tissues collected as part of our study further confirmed this correlation. In vitro experiments demonstrated that over-expression of CLCA4 could inhibit cell migration and invasion by suppressing epithelial-mesenchymal transition (EMT) via PI3K/ATK signaling and change the expression patterns of EMT markers in CLCA4-gain-of-function cell models. CONCLUSIONS CLCA4 inhibits migration and invasion by suppressing EMT via PI3K/ATK signaling and predicts favorable prognosis of CRC which may help to distinguish potential risk of lymph node metastasis in CRC.

Indexed as

CalciumCell Line, TumorCell MovementCell ProliferationChloride ChannelsColorectal NeoplasmsDatabases, GeneticDisease ProgressionEpithelial-Mesenchymal TransitionFemaleHumansKaplan-Meier EstimateMaleMiddle AgedNeoplasm InvasivenessPhosphatidylinositol 3-KinasesCalciumChloride ChannelsCLCA4 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID31164625
PMCPMC6563650
OpenAlexW2980820582

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.