Evidence map›Paper›PMID 32240440›Full record

ArticleInternational journal of clinical oncology2020

Inhibition of TMEM16A suppresses growth and induces apoptosis in hepatocellular carcinoma.

Chuantao Zhang, Jianxiang Liu, Zhiyi Han, Xiang Cui, Deti Peng, Yufeng Xing

RetractedAbstract readRetracted Publication
PubMed Publisher
In one paragraph

Article in International journal of clinical oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 11 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 2 pooled it
0.9field-weighted citation impact, top 27% 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

11 citing papers in PubMed, 2 syntheses or guidelines pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Role of ANO1 in tumors and tumor immunity.Journal of cancer research and clinical oncology · 2022
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. The CaActa pharmaceutica Sinica. B · 2021
    Review
  11. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Chuantao Zhang *Department of Respiration, Hospital of Chengdu university of Traditional Chinese Medicine, Chengdu, 610072, Sichuan, China.
Jianxiang Liu *Key Laboratory of Medicinal Biotechnology, Guilin Medical University, Guilin, 541004, Guangxi, China.
Zhiyi HanDepartment of Hepatology, Shenzhen Traditional Chinese Medicine Hospital, NO.1, Fuhua Road, Futian District, Shenzhen, 518033, Guangdong, China.
Xiang CuiDepartment of Hepatology, Shenzhen Traditional Chinese Medicine Hospital, NO.1, Fuhua Road, Futian District, Shenzhen, 518033, Guangdong, China.
Deti PengDepartment of Hepatology, Shenzhen Traditional Chinese Medicine Hospital, NO.1, Fuhua Road, Futian District, Shenzhen, 518033, Guangdong, China.
Yufeng XingDepartment of Hepatology, Shenzhen Traditional Chinese Medicine Hospital, NO.1, Fuhua Road, Futian District, Shenzhen, 518033, Guangdong, China. yufeng000729@163.com.
Shenzhen Pingle Orthopedic Hospital · CNChengdu University of Traditional Chinese Medicine · CNGuilin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncrease of the Ca

methodsIn the present study, the expression of TMEM16A in hepatocellular carcinoma (HCC) tissues were measured by quantitative reverse-transcription polymerase chain reaction (qRT-PCR), Western blot and immunohistochemical. Cell proliferation was detected using CCK-8, EdU staining and colony formation methods. Flow cytometry was carried out for detecting cell cycle distribution and apoptosis rate. Migration and invasion abilities were analyzed using transwell and wound healing assay. Western blot method was performed to analyze protein expression.

resultsHere, we found TMEM16A was significantly increased in HCC tissues, and a higher TMEM16A expression levels were detected in larger tumor size, higher tumor grade, with distant metastasis and poor differentiation. Moreover, overexpression of TMEM16A promoted HCC growth, migration and invasion, and suppressed apoptosis in vitro and in vivo. Knockdown of TMEM16A inhibited HCC growth, migration and invasion, and induced apoptosis in vitro and in vivo. Furthermore, TMEM16A regulated PI3K/AKT-MAKP signaling pathway.

conclusionOur data indicate that TMEM16A may represent a novel biomarker of HCC and may be a potential therapeutic target for diagnosis and therapy.

Indexed as

ApoptosisAnimalsAnoctamin-1Carcinoma, HepatocellularCell CycleCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMaleMAP Kinase Signaling SystemMice, Inbred BALB CNeoplasm ProteinsPhosphatidylinositol 3-KinasesANO1 protein, humanAnoctamin-1Neoplasm ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktCell proliferationHCCPI3K/AKT-MAKPTMEM16ATumorigenesis

Identifiers

PMID32240440
OpenAlexW3014749283

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.