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The expression of long noncoding RNA CRCAL-3 in colorectal cancer and its impacts on cell proliferation and migration.
Chang, Hui; Wang, Guan-Nan; Tao, Ya-Lan.
Afiliación
  • Chang H; Department of Radiation Oncology, Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, Guangdong, China.
  • Wang GN; Department of Radiation Oncology, Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, Guangdong, China.
  • Tao YL; Department of Radiation Oncology, Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, Guangdong, China.
J Cell Biochem ; 120(9): 15369-15377, 2019 09.
Article en En | MEDLINE | ID: mdl-31038794
ABSTRACT
Long noncoding RNAs (lncRNAs) have been implicated in colorectal cancer (CRC). And lncRNA RP11-138J23.1 (CRCAL-3) was previously reported as a candidate regulator of CRC development. But its regulating functions have not been fully elucidated. Here, we analyzed RNA sequencing data from the Cancer Genome Atlas (TCGA) and 253 CRC patients treated in our hospital to assess expression dysregulation of CRCAL-3, and the correlation between CRCAL-3 expression and disease progression. Further, polymerase chain reaction (PCR) assay on different cell lines and knockdown experiments by small interfering RNA were performed to assess functions of CRCAL-3 in proliferation and migration of CRC cells. As a result, analyses on TCGA datasets showed an upregulated CRCAL-3 expression in 14 solid tumors, including CRC. PCR assay on 253 cases of CRC tissue and 114 cases of normal adjacent tissue confirmed this expression upregulation. Also, CRCAL-3 expression was exhibited by survival analyses on the 253 CRC patients, to have a negative correlation with patients' overall and progression-free survivals. PCR assay on different cell lines showed that CRC cells expressed a higher level of CRCAL-3, compared with normal colonic epithelial cells. In vitro knockdown of CRCAL-3 resulted in an obvious retardation of proliferation and migration in two CRC cell lines (HCT116 and DLD-1). Moreover, CRCAL-3 knockdown was observed in xenograft models to repress cell proliferation and enhance cisplatin sensitivity. Taking these results together, CRCAL-3 emerged as a biomarker for early diagnosis, prognosis prediction, and individualized treatment of CRC.
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Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Neoplasias Colorrectales / Regulación hacia Arriba / Perfilación de la Expresión Génica / ARN Largo no Codificante Tipo de estudio: Prognostic_studies / Screening_studies Límite: Animals / Female / Humans / Male Idioma: En Revista: J Cell Biochem Año: 2019 Tipo del documento: Article País de afiliación: China

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Neoplasias Colorrectales / Regulación hacia Arriba / Perfilación de la Expresión Génica / ARN Largo no Codificante Tipo de estudio: Prognostic_studies / Screening_studies Límite: Animals / Female / Humans / Male Idioma: En Revista: J Cell Biochem Año: 2019 Tipo del documento: Article País de afiliación: China