Evidence map›Paper›PMID 33760180›Full record

ArticleMolecular medicine reports2021

Galectin‑3 facilitates the proliferation and migration of nasopharyngeal carcinoma cells via activation of the ERK1/2 and Akt signaling pathways, and is positively correlated with the inflammatory state of nasopharyngeal carcinoma.

Mei Li, Yu Bin Chen, Fen Liu, Jia Quan Qu, Li Cheng Ren, Jin Chai, Can E Tang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 44% 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

6 citing papers in PubMed, 7 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

7 authors at 3 institutions in 1 country.

Mei Li *Institute of Medical Science Research, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Yu Bin Chen *Department of Cardiac Surgery, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Fen LiuInstitute of Medical Science Research, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Jia Quan QuCholestatic Liver Diseases Center and Department of Gastroenterology, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Li Cheng RenDepartment of Burn and Reconstructive Surgery, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Jin ChaiCholestatic Liver Diseases Center and Department of Gastroenterology, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Can E TangInstitute of Medical Science Research, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
Central South University · CNArmy Medical University · CNXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nasopharyngeal carcinoma (NPC) is an epithelial carcinoma originating from the nasopharyngeal mucosal tissue and is highly prevalent in southeast Asia. Galectin‑3 (gal‑3) serves crucial roles in many cancers but its role in NPC remains to be elucidated. The aim of the present study was to investigate the role of gal‑3 in NPC. Immunohistochemistry and ELISA were used to determine the expression level of gal‑3 in patients with NPC or chronic rhinitis (CR). Gal‑3 short hairpin (sh)RNA was established to knockdown gal‑3 in 5‑8F and 6‑10B cells, allowing for the evaluation of the roles of gal‑3 in proliferation, migration and apoptosis in NPC cell lines. Immunohistochemistry staining of IL‑6 and IL‑8 was applied to access the inflammatory state of tumor tissues, and the correlation between the inflammatory state and gal‑3 was analyzed. The results demonstrated that gal‑3 was upregulated in patients with NPC compared with patients with CR. Knockdown of gal‑3 inhibited proliferation and migration in 5‑8F and 6‑10B cells, as well as promoted apoptosis in these cells. The expression levels of MMP‑9 and IL‑8 were also decreased in 5‑8F and 6‑10B cells after transfection with gal‑3 shRNA. A positive correlation was identified between the expression level of gal‑3 and the inflammatory state of NPC. The phosphorylation levels of ERK1/2 and Akt were downregulated after knockdown of gal‑3 in 5‑8F and 6‑10B cells. In conclusion, the expression level of gal‑3 was upregulated in patients with NPC and was positively correlated with the inflammatory state of NPC. The results suggested that gal‑3 promoted the proliferation and migration of 5‑8F and 6‑10B cells, while inhibiting the apoptosis of these cells. Moreover, activation of ERK1/2 and Akt may be the underlying mechanism of the effects of gal‑3 on NPC.

Indexed as

ApoptosisCell Line, TumorCell MovementCell ProliferationFemaleGalectin 3Gene Expression Regulation, NeoplasticHumansInflammationInterleukin-8MaleMAP Kinase Signaling SystemMatrix Metalloproteinase 9Middle AgedNasopharyngeal CarcinomaOncogene Protein v-aktCXCL8 protein, humanGalectin 3Interleukin-8Matrix Metalloproteinase 9MMP9 protein, humanOncogene Protein v-aktRNA, Small InterferingAktERK1/2galectin‑3inflammationnasopharyngeal carcinoma

Identifiers

PMID33760180
PMCPMC7986014
OpenAlexW3136828675

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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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 Socratic graph.