Evidence map›Paper›PMID 34082790›Full record

ArticleHead & face medicine2021

ANLN promotes carcinogenesis in oral cancer by regulating the PI3K/mTOR signaling pathway.

Bing Wang, Xiao-Li Zhang, Chen-Xi Li, Ning-Ning Liu, Min Hu, Zhong-Cheng Gong

Open access · goldAbstract read
In one paragraph

Article in Head & face medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

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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 3 institutions in 1 country.

Bing Wang *Oncological Department of Oral and Maxillofacial Surgery, Xinjiang Medical University Affiliated First Hospital, Stomatological School of Xinjiang Medical University, Stomatology Research Institute of Xinjiang Province, No.137 Liyushan South Road, 830054, Urumqi, PR China.
Xiao-Li Zhang *People's Hospital of Xinjiang Uygur Autonomous Region, 830001, Urumqi, PR China.
Chen-Xi Li *Oncological Department of Oral and Maxillofacial Surgery, Xinjiang Medical University Affiliated First Hospital, Stomatological School of Xinjiang Medical University, Stomatology Research Institute of Xinjiang Province, No.137 Liyushan South Road, 830054, Urumqi, PR China. lichenxi89@yahoo.com.
Ning-Ning LiuDepartment of Prosthodontia, Xinjiang Medical University Affiliated First Hospital, 830054, Urumqi, PR China.
Min HuUrumqi Myour Dental Clinic, 830002, Urumqi, PR China.
Zhong-Cheng GongOncological Department of Oral and Maxillofacial Surgery, Xinjiang Medical University Affiliated First Hospital, Stomatological School of Xinjiang Medical University, Stomatology Research Institute of Xinjiang Province, No.137 Liyushan South Road, 830054, Urumqi, PR China. gump0904@aliyun.com.
Xinjiang Medical University · CNFirst Affiliated Hospital of Xinjiang Medical University · CNPeople's Hospital of Xinjiang Uygur Autonomous Region · CN

Funding

National Natural Science Foundation of China 81760191Xinjiang Special Scientific Research Project of Youth Medical Science and Technology WJWY-201924
6 · The paper itself

Abstract

backgroundOral cancer is a malignant disease that threatenshuman life and greatly reducespatientquality of life. ANLN was reported to promote the progression of cancer. This study aims to investigate the role of ANLNin oral cancer and the underlying molecular mechanism.

methodsANLN expression was downregulated by RNAi technology. The effect of ANLN on cell behaviors, including proliferation, cell cycle progression, invasion, and apoptosis, was detected. Western blotting analysis was used to explore the mechanism by whichANLN functions in oral cancer.

resultsData from TCGA database showed that ANLN was expressed at significantly higher levels in tumor tissues thanin normal control tissues. Patients with higher ANLN expression exhibitedshorter survivaltimes. ANLN was alsoabundantly expressedin the cancer cell lines CAL27 and HN30. When ANLN was knocked down in CAL27 and HN30 cells, cell proliferation and colony formation weredecreased. The cell invasion ability was also inhibited. However, the cell apoptosis rate was increased. In addition, the levels of critical members of the PI3K signaling pathway, includingPI3K, mTOR, Akt, and PDK-1, were significantlyreducedafter ANLN was knocked down in CAL27 cells.

conclusionsANLN contributes to oral cancerprogressionand affects activation ofthe PI3K/mTOR signaling pathway. This study providesa new potential targetfor drug development and treatment in oral cancer.

Indexed as

Mouth NeoplasmsPhosphatidylinositol 3-KinasesSignal TransductionCarcinogenesisCell Line, TumorCell ProliferationHumansMicrofilament ProteinsProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesANLN protein, humanMicrofilament ProteinsMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesANLNmTOROral cancerPI3K signaling pathway

Identifiers

PMID34082790
PMCPMC8173900
OpenAlexW3164202848

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.