Evidence map›Paper›PMID 34208068›Full record

ArticleCancers2021

MITF Promotes Cell Growth, Migration and Invasion in Clear Cell Renal Cell Carcinoma by Activating the RhoA/YAP Signal Pathway.

Nayoung Kim, Solbi Kim, Myung-Won Lee, Heung-Jin Jeon, Hyewon Ryu, Jin-Man Kim, Hyo-Jin Lee

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-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

21 citing papers in PubMed, 26 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 1 institution in 1 country.

Nayoung KimDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon 34134, Korea.
Solbi KimDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon 34134, Korea.
Myung-Won LeeDepartment of Internal Medicine, College of Medicine, Chungnam National University, Daejeon 34134, Korea.ORCID 0000-0003-2787-5256
Heung-Jin JeonInfection Control Convergence Research Center, College of Medicine, Chungnam National University, Daejeon 34134, Korea.ORCID 0000-0001-8704-3713
Hyewon RyuDepartment of Internal Medicine, College of Medicine, Chungnam National University, Daejeon 34134, Korea.ORCID 0000-0001-9313-9930
Jin-Man KimDepartment of Pathology, College of Medicine, Chungnam National University, Daejeon 34134, Korea.
Hyo-Jin LeeDepartment of Medical Science, College of Medicine, Chungnam National University, Daejeon 34134, Korea.ORCID 0000-0001-8378-3001
Chungnam National University · KR

Funding

Korea Health Industry Development Institute HR20C0025National Research Foundation of Korea NRF-2017R1D1A1B04034638, NRF-2017R1A5A2015385
6 · The paper itself

Abstract

Microphthalmia-associated transcription factor (MITF) is a basic helix-loop-helix leucine zipper transcription factor involved in the lineage-specific regulation of melanocytes, osteoclasts and mast cells. MITF is also involved in the progression of melanomas and other carcinomas, including the liver, pancreas and lung. However, the role of MITF in clear cell renal cell carcinoma (ccRCC) is largely unknown. This study investigates the functional role of MITF in cancer and the molecular mechanism underlying disease progression in ccRCC. MITF knockdown inhibited cell proliferation and shifted the cell cycle in ccRCC cells. In addition, MITF knockdown reduced wound healing, cell migration and invasion compared with the controls. Conversely, MITF overexpression in SN12C and SNU482 cells increased cell migration and invasion. Overexpression of MITF activated the RhoA/YAP signaling pathway, which regulates cell proliferation and invasion, and increased YAP signaling promoted cell cycle-related protein expression. Additionally, tumor formation was impaired by MITF knockdown and enhanced by MITF overexpression in vivo. In summary, MITF expression was associated with aggressive tumor behavior, and increased the migratory and invasive capabilities of ccRCC cells. These effects were reversed by MITF suppression. These results suggest that MITF is a potential therapeutic target for the treatment of ccRCC.

Indexed as

cell cycleinvasionmigrationMITFproliferationrenal cell carcinomaRhoAYAP

Identifiers

PMID34208068
PMCPMC8230652
OpenAlexW3169679792

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.