Evidence map›Paper›PMID 31118065›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

miR-let-7b and miR-let-7c suppress tumourigenesis of human mucosal melanoma and enhance the sensitivity to chemotherapy.

Huan Tang, Meng Ma, Jie Dai, Chuanliang Cui, Lu Si, Xinan Sheng, Zhihong Chi, Longwen Xu, Sifan Yu, Tianxiao Xu and 5 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing 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

40 citing papers in PubMed, 59 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

15 authors at 2 institutions in 1 country.

Huan TangDepartment of Renal Cancer and Melanoma, Peking University Cancer Hospital & Institute, 52 Fucheng Road, Beijing, 100142, China.
Meng MaDepartment of Renal Cancer and Melanoma, Peking University Cancer Hospital & Institute, 52 Fucheng Road, Beijing, 100142, China.
Jie DaiDepartment of Renal Cancer and Melanoma, Peking University Cancer Hospital & Institute, 52 Fucheng Road, Beijing, 100142, China.
Chuanliang CuiDepartment of Renal Cancer and Melanoma, Peking University Cancer Hospital & Institute, 52 Fucheng Road, Beijing, 100142, China.
Lu SiDepartment of Renal Cancer and Melanoma, Peking University Cancer Hospital & Institute, 52 Fucheng Road, Beijing, 100142, China.
Xinan ShengDepartment of Renal Cancer and Melanoma, Peking University Cancer Hospital & Institute, 52 Fucheng Road, Beijing, 100142, China.
Zhihong ChiDepartment of Renal Cancer and Melanoma, Peking University Cancer Hospital & Institute, 52 Fucheng Road, Beijing, 100142, China.
Longwen XuDepartment of Renal Cancer and Melanoma, Peking University Cancer Hospital & Institute, 52 Fucheng Road, Beijing, 100142, China.
Sifan YuDepartment of Renal Cancer and Melanoma, Peking University Cancer Hospital & Institute, 52 Fucheng Road, Beijing, 100142, China.
Tianxiao XuDepartment of Renal Cancer and Melanoma, Peking University Cancer Hospital & Institute, 52 Fucheng Road, Beijing, 100142, China.
Junya YanDepartment of Renal Cancer and Melanoma, Peking University Cancer Hospital & Institute, 52 Fucheng Road, Beijing, 100142, China.
Huan YuDepartment of Renal Cancer and Melanoma, Peking University Cancer Hospital & Institute, 52 Fucheng Road, Beijing, 100142, China.
Lu YangDepartment of Renal Cancer and Melanoma, Peking University Cancer Hospital & Institute, 52 Fucheng Road, Beijing, 100142, China.
Yan KongDepartment of Renal Cancer and Melanoma, Peking University Cancer Hospital & Institute, 52 Fucheng Road, Beijing, 100142, China. kyan08@bjmu.edu.cn.
Jun GuoDepartment of Renal Cancer and Melanoma, Peking University Cancer Hospital & Institute, 52 Fucheng Road, Beijing, 100142, China. guoj307@126.com.
Peking University Cancer Hospital · CNPeking University · CN

Funding

Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding Support ZYLX201603Beijing Talents Foundation 2016000021223ZK18Fostering Young Scholars of Peking University Health Science Center, Beijing Baiqianwan Talents Project and Beijing Municipal Administration of Hospitals' Ascent Plan DFL20181101National Natural Science Foundation of China 81672696National Natural Science Foundation of China 81772912
6 · The paper itself

Abstract

backgroundMucosal melanoma with poor prognosis is a common histopathologic subtype of melanoma among Chinese and other Asian peoples. Regulated microRNAs (miRNAs) have been reported as oncogenes or tumour suppressors in melanoma. However, the roles of specific miRNAs in mucosal melanoma remain largely unknown. Here, we aimed to assess the biological functions, molecular mechanisms and clinical potential of miR-let-7b and miR-let-7c in mucosal melanoma.

methodsThe expression of miR-let-7b and miR-let-7c in mucosal melanoma was determined by quantitative polymerase chain reaction (qPCR). Cutoff scores for miR-let-7b and miR-let-7c expressions were calculated through receiver operating characteristic (ROC) curve analysis in 106 mucosal melanoma patients according to recurrence. Correlations of miR-let-7b and miR-let-7c expression with clinicopathological characteristics, disease-free survival (DFS) and clinical benefits after treatment were then statistically analysed. The biological functions and molecular mechanisms of miR-let-7b and miR-let-7c were studied in vitro and in vivo.

resultsThe expression of miR-let-7b and miR-let-7c was decreased in 94 cases (88.7%) and 89 cases (84.0%) of 106 mucosal melanoma patients compared with mucosal nevi. A correlation was observed between the expression of miR-let-7b, miR-let-7c and DFS after surgery. In addition, overexpression of miR-let-7b or miR-let-7c inhibited mucosal melanoma cell growth, migration, invasion and metastasis and induced cell apoptosis and cell cycle arrest in vitro and in vivo. Mechanistically, miR-let-7b and miR-let-7c directly targeted metadherin (MTDH) and calumenin (CALU) and suppressed phospho-ERK in mucosal melanoma cells. MTDH and CALU reversed the partial function of miR-let-7b and miR-let-7c in vitro. Furthermore, progression-free survival (PFS) of mucosal melanoma patients upon temozolomide-based and paclitaxel-based chemotherapy was related to miR-let-7b and miR-let-7c expression. Overexpression of miR-let-7b or miR-let-7c in patient-derived xenograft (PDX) models and certain mucosal melanoma cells had better growth inhibition after temozolomide and paclitaxel treatment. MTDH reversed the sensitivity of miR-let-7b and miR-let-7c to paclitaxel in vitro.

conclusionsOur results suggested that miR-let-7b and miR-let-7c inhibited the recurrence of mucosal melanoma through inhibiting cell growth, migration, invasion and metastasis, inducing cell apoptosis and cell cycle arrest by targeting MTDH and CALU. In addition, miR-let-7b and miR-let-7c increased sensitivity to chemotherapeutic agents by targeting MTDH.

Indexed as

AgedAnimalsApoptosisCalcium-Binding ProteinsCarcinogenesisCell Adhesion MoleculesCell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationDisease-Free SurvivalFemaleGene Expression Regulation, NeoplasticHumansMaleMelanomaCalcium-Binding ProteinsCALU protein, humanCell Adhesion MoleculesMembrane ProteinsMicroRNAsmirnlet7 microRNA, humanMTDH protein, humanPaclitaxelRNA-Binding ProteinsChemotherapymiR-let-7bmiR-let-7cMucosal melanoma

Identifiers

PMID31118065
PMCPMC6532197
OpenAlexW2947198834

What OpenQuestion holds

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LicenceCC BY
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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.