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Yonsei Med J. 2019 Apr;60(4):326-335. doi: 10.3349/ymj.2019.60.4.326.

Potential Oncogenic Role of the Papillary Renal Cell Carcinoma Gene in Non-Small Cell Lung Cancers.

Jang SH1,2,3,4, Jiang Y4,5, Shin S2,3,4, Jung SH2,3,6, Jung CK7, Chung YJ1,2,3,8.

Author information

1
Molecular Cell Biology, Department of Biomedicine & Health Sciences, The Catholic University of Korea, Seoul, Korea.
2
Precision Medicine Research Center, College of Medicine, The Catholic University of Korea, Seoul, Korea.
3
Integrated Research Center for Genome Polymorphism, College of Medicine, The Catholic University of Korea, Seoul, Korea.
4
Department of Microbiology, College of Medicine, The Catholic University of Korea, Seoul, Korea.
5
Department of Immunology, Medicine & Pharmacy Research Center, Binzhou Medical University, Yantai, China.
6
Cancer Evolution Research Center, The Catholic University of Korea, Seoul, Korea.
7
Department of Hospital Pathology, College of Medicine, The Catholic University of Korea, Seoul, Korea.
8
Department of Microbiology, College of Medicine, The Catholic University of Korea, Seoul, Korea. yejun@catholic.ac.kr.

Abstract

PURPOSE:

Papillary renal cell carcinoma (PRCC) gene, which located in 1q23.1, is recurrently amplified in non-small cell lung cancer (NSCLC). However, it is unknown whether PRCC is overexpressed in primary NSCLCs and whether PRCC overexpression contributes to lung tumorigenesis. In this study, we aimed to identify the profiles of PRCC expression in Korean NSCLC patients and to elucidate the role of PRCC overexpression on lung tumorigenesis.

MATERIALS AND METHODS:

We performed immunohistochemistry analysis with a tissue array containing 161 primary NSCLCs. Small interfering RNA targeting PRCC (siPRCC) was transfected into two lung cancer cell lines (NCI-H358 and A549), after which tumor growth, migration, and invasion were observed. Expressions of cell proliferation-, cell cycle-, and metastasis-related molecules were examined by Western blot analysis. We also explored the in vivo effect of PRCC silencing.

RESULTS:

PRCC overexpression was recurrently observed in NSCLCs (95/161, 59%). After siPRCC treatment, tumor cell proliferation, colony formation, and anchorage independent growth were significantly reduced (p<0.001 for all three effects). Migration and invasiveness were also significantly repressed (p<0.001 for both effects). Reflecting cell proliferation, cell cycle, and metastasis, the expressions of Ki67, cyclin D1, AKT-1, pAKT, NF-kB p65, vimentin and CXCL-12 were found to be downregulated. Through mouse xenograft analysis, we confirmed that PRCC silencing significantly repressed a xenograft tumor mass in vivo (p<0.001).

CONCLUSION:

The present data provide evidence that PRCC overexpression is involved in the tumorigenesis and progression of lung cancer.

KEYWORDS:

Lung cancer; PRCC; overexpression; siRNA

PMID:
30900418
PMCID:
PMC6433567
DOI:
10.3349/ymj.2019.60.4.326
[Indexed for MEDLINE]
Free PMC Article

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