Evidence map›Paper›PMID 35578316›Full record

ArticleBMC cancer2022

SCARA3 inhibits cell proliferation and EMT through AKT signaling pathway in lung cancer.

Jeeho Kim, Ho Jin You, Chakyung Youn

Abstract read
In one paragraph

Article in BMC cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

10 citing papers in PubMed.

  1. Article
  2. EMT and cancer stem cells: Drivers of therapy resistance and promising therapeutic targets.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. [miR-2110 Affects the Biological Behaviors of Lung Adenocarcinoma by Regulating CDT1].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024
    Article
  8. Article
  9. Article
  10. Article
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

3 authors.

Jeeho KimLaboratory of Genomic Instability and Cancer therapeutics and Department of Pharmacology, Chosun University School of Medicine, 375 Seosuk-Dong, Gwangju, 501-759, South Korea.
Ho Jin YouLaboratory of Genomic Instability and Cancer therapeutics and Department of Pharmacology, Chosun University School of Medicine, 375 Seosuk-Dong, Gwangju, 501-759, South Korea. hjyou@chosun.ac.kr.
Chakyung YounDepartment of Meridian & Acupoint∙Diagnosis College of Korean Medicine, Dongshin University 67, Dongsindae-gil, Naju-si, Jeollanam-do, Republic of Korea. threefold@hanmail.net.

Funding

Chakyung Youn NRF-2017R1A2B1008687Ho Jin You NRF-2015R1A5A2009070
6 · The paper itself

Abstract

backgroundScavenger receptor class A member 3 (SCARA3) is decreased in prostate cancer and myeloma. However, functions of SCARA3 in various cancers remain unclear. In this study, we tried to evaluate the functional study of SCARA3 in lung cancer.

methodsThe expression level of SCARA3 in the TCGA-database, lung cancer tissue microarray and lung cancer cells and the prognosis of lung cancer patients were measured. Lung cancer tissue microarray was analyzed pathologically using immunohistochemistry, and quantitative analysis of SCARA3 in normal lung cells and lung cancer cells was analyzed using western blot analysis. Survival curves for lung cancer patients were prepared with the Kaplan-Meier method. Migration and invasion of SCARA3 overexpressed lung cancer cells were determined using a Transwell chamber system. Proliferation of lung cancer cells was determined based on cell viability assay using cell culture in vitro and a tumorigenicity model of BALB/C nude mouse in vivo.

resultsThe expression of SCARA3 was abnormally reduced in TCGA-database, lung tissue microarray, and various lung cancer cells. However, overexpression of SCARA3 reduced the proliferation of lung cancer. The ability of SCARA3 to inhibit cancer cell proliferation was maintained even in vivo using a mouse xenograft model. In addition, overexpression of SCARA3 reduced migration and invasion ability of lung cancer cells and induced decreases of EMT markers such as β-catenin, vimentin, and MMP9. We aimed to prove the role of SCARA3 in the treatment of Lung cancer, and shown that the expression level of SCARA3 is important in cancer treatment using cisplatin. The enhancement of the effect of cisplatin according to SCARA3 overexpression is via the AKT and JNK pathways.

conclusionsThis study confirmed an abnormal decrease in SCARA3 in lung cancer. Overexpression of SCARA3 potently inhibited tumors in lung cancer and induced apoptosis by increasing sensitivity of lung cancer to cisplatin. These results suggest that SCARA3 is a major biomarker of lung cancer and that the induction of SCARA3 overexpression can indicate an effective treatment.

Indexed as

Lung NeoplasmsProto-Oncogene Proteins c-aktAnimalsCell Line, TumorCell MovementCell ProliferationCisplatinEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHeat-Shock ProteinsHumansMaleMiceMice, Inbred BALB CScavenger Receptors, Class ASignal TransductionCisplatinHeat-Shock ProteinsProto-Oncogene Proteins c-aktSCARA3 protein, humanScavenger Receptors, Class AAKT signalingLung CancerSCARA3Tumor growth

Identifiers

PMID35578316
PMCPMC9112459

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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 OpenQuestion graph.