miR-204-5p inhibits proliferation and invasion and enhances chemotherapeutic sensitivity of colorectal cancer cells by downregulating RAB22A
miR-204-5p was found to be downregulated in colorectal cancer tissues in our preliminary microarray analyses. However, the function of miR-204-5p in colorectal cancer remains unknown. We therefore investigated the role, mechanism, and clinical significance of miR-204-5p in colorectal cancer developm...
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| Veröffentlicht in: | Clinical cancer research Jg. 20; H. 23; S. 6187 |
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| Abstract | miR-204-5p was found to be downregulated in colorectal cancer tissues in our preliminary microarray analyses. However, the function of miR-204-5p in colorectal cancer remains unknown. We therefore investigated the role, mechanism, and clinical significance of miR-204-5p in colorectal cancer development and progression.
We measured the expression of miR-204-5p and determined its correlation with patient prognoses. Ectopic expression in colorectal cancer cells, xenografts, and pulmonary metastasis models was used to evaluate the effects of miR-204-5p on proliferation, migration, and chemotherapy sensitivity. Luciferase assay and Western blotting were performed to validate the potential targets of miR-204-5p after the preliminary screening by a microarray analysis and computer-aided algorithms.
miR-204-5p is frequently downregulated in colorectal cancer tissues, and survival analysis showed that the downregulation of miR-204-5p in colorectal cancer was associated with poor prognoses. Ectopic miR-204-5p expression repressed colorectal cancer cell growth both in vitro and in vivo. Moreover, restoring miR-204-5p expression inhibited colorectal cancer migration and invasion and promoted tumor sensitivity to chemotherapy. Mechanistic investigations revealed that RAB22A, a member of the RAS oncogene family, is a direct functional target of miR-204-5p in colorectal cancer. Furthermore, RAB22A protein levels in colorectal cancer tissues were frequently increased and negatively associated with miR-204-5p levels and survival time.
Our results demonstrate for the first time that miR-204-5p acts as a tumor suppressor in colorectal cancer through inhibiting RAB22A and reveal RAB22A to be a new oncogene and prognostic factor for colorectal cancer. |
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| AbstractList | miR-204-5p was found to be downregulated in colorectal cancer tissues in our preliminary microarray analyses. However, the function of miR-204-5p in colorectal cancer remains unknown. We therefore investigated the role, mechanism, and clinical significance of miR-204-5p in colorectal cancer development and progression.PURPOSEmiR-204-5p was found to be downregulated in colorectal cancer tissues in our preliminary microarray analyses. However, the function of miR-204-5p in colorectal cancer remains unknown. We therefore investigated the role, mechanism, and clinical significance of miR-204-5p in colorectal cancer development and progression.We measured the expression of miR-204-5p and determined its correlation with patient prognoses. Ectopic expression in colorectal cancer cells, xenografts, and pulmonary metastasis models was used to evaluate the effects of miR-204-5p on proliferation, migration, and chemotherapy sensitivity. Luciferase assay and Western blotting were performed to validate the potential targets of miR-204-5p after the preliminary screening by a microarray analysis and computer-aided algorithms.EXPERIMENTAL DESIGNWe measured the expression of miR-204-5p and determined its correlation with patient prognoses. Ectopic expression in colorectal cancer cells, xenografts, and pulmonary metastasis models was used to evaluate the effects of miR-204-5p on proliferation, migration, and chemotherapy sensitivity. Luciferase assay and Western blotting were performed to validate the potential targets of miR-204-5p after the preliminary screening by a microarray analysis and computer-aided algorithms.miR-204-5p is frequently downregulated in colorectal cancer tissues, and survival analysis showed that the downregulation of miR-204-5p in colorectal cancer was associated with poor prognoses. Ectopic miR-204-5p expression repressed colorectal cancer cell growth both in vitro and in vivo. Moreover, restoring miR-204-5p expression inhibited colorectal cancer migration and invasion and promoted tumor sensitivity to chemotherapy. Mechanistic investigations revealed that RAB22A, a member of the RAS oncogene family, is a direct functional target of miR-204-5p in colorectal cancer. Furthermore, RAB22A protein levels in colorectal cancer tissues were frequently increased and negatively associated with miR-204-5p levels and survival time.RESULTSmiR-204-5p is frequently downregulated in colorectal cancer tissues, and survival analysis showed that the downregulation of miR-204-5p in colorectal cancer was associated with poor prognoses. Ectopic miR-204-5p expression repressed colorectal cancer cell growth both in vitro and in vivo. Moreover, restoring miR-204-5p expression inhibited colorectal cancer migration and invasion and promoted tumor sensitivity to chemotherapy. Mechanistic investigations revealed that RAB22A, a member of the RAS oncogene family, is a direct functional target of miR-204-5p in colorectal cancer. Furthermore, RAB22A protein levels in colorectal cancer tissues were frequently increased and negatively associated with miR-204-5p levels and survival time.Our results demonstrate for the first time that miR-204-5p acts as a tumor suppressor in colorectal cancer through inhibiting RAB22A and reveal RAB22A to be a new oncogene and prognostic factor for colorectal cancer.CONCLUSIONSOur results demonstrate for the first time that miR-204-5p acts as a tumor suppressor in colorectal cancer through inhibiting RAB22A and reveal RAB22A to be a new oncogene and prognostic factor for colorectal cancer. miR-204-5p was found to be downregulated in colorectal cancer tissues in our preliminary microarray analyses. However, the function of miR-204-5p in colorectal cancer remains unknown. We therefore investigated the role, mechanism, and clinical significance of miR-204-5p in colorectal cancer development and progression. We measured the expression of miR-204-5p and determined its correlation with patient prognoses. Ectopic expression in colorectal cancer cells, xenografts, and pulmonary metastasis models was used to evaluate the effects of miR-204-5p on proliferation, migration, and chemotherapy sensitivity. Luciferase assay and Western blotting were performed to validate the potential targets of miR-204-5p after the preliminary screening by a microarray analysis and computer-aided algorithms. miR-204-5p is frequently downregulated in colorectal cancer tissues, and survival analysis showed that the downregulation of miR-204-5p in colorectal cancer was associated with poor prognoses. Ectopic miR-204-5p expression repressed colorectal cancer cell growth both in vitro and in vivo. Moreover, restoring miR-204-5p expression inhibited colorectal cancer migration and invasion and promoted tumor sensitivity to chemotherapy. Mechanistic investigations revealed that RAB22A, a member of the RAS oncogene family, is a direct functional target of miR-204-5p in colorectal cancer. Furthermore, RAB22A protein levels in colorectal cancer tissues were frequently increased and negatively associated with miR-204-5p levels and survival time. Our results demonstrate for the first time that miR-204-5p acts as a tumor suppressor in colorectal cancer through inhibiting RAB22A and reveal RAB22A to be a new oncogene and prognostic factor for colorectal cancer. |
| Author | Yu, Jian Quan, Chao Mao, Yong Zhou, Leyuan Du, Xiang Fei, Bojian Hu, Yaling Yin, Yuan Wang, Qifeng Song, Mingxu Zhang, Binbin Hua, Dong Bian, Zehua Wang, Weili Zhang, Jiwei Ni, Shujuan Wang, Yugang Huang, Zhaohui |
| Author_xml | – sequence: 1 givenname: Yuan surname: Yin fullname: Yin, Yuan organization: Wuxi Oncology Institute, the Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China – sequence: 2 givenname: Binbin surname: Zhang fullname: Zhang, Binbin organization: Wuxi Oncology Institute, the Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China. Oncology Institute, the Fourth Affiliated Hospital of Soochow University, Wuxi, Jiangsu, China – sequence: 3 givenname: Weili surname: Wang fullname: Wang, Weili organization: Department of Surgical Oncology, the Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China – sequence: 4 givenname: Bojian surname: Fei fullname: Fei, Bojian organization: Department of Surgical Oncology, the Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China – sequence: 5 givenname: Chao surname: Quan fullname: Quan, Chao organization: Wuxi Oncology Institute, the Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China – sequence: 6 givenname: Jiwei surname: Zhang fullname: Zhang, Jiwei organization: Wuxi Oncology Institute, the Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China – sequence: 7 givenname: Mingxu surname: Song fullname: Song, Mingxu organization: Wuxi Oncology Institute, the Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China – sequence: 8 givenname: Zehua surname: Bian fullname: Bian, Zehua organization: Wuxi Oncology Institute, the Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China – sequence: 9 givenname: Qifeng surname: Wang fullname: Wang, Qifeng organization: Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai, China – sequence: 10 givenname: Shujuan surname: Ni fullname: Ni, Shujuan organization: Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai, China – sequence: 11 givenname: Yaling surname: Hu fullname: Hu, Yaling organization: Wuxi Oncology Institute, the Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China – sequence: 12 givenname: Yong surname: Mao fullname: Mao, Yong organization: Wuxi Oncology Institute, the Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China – sequence: 13 givenname: Leyuan surname: Zhou fullname: Zhou, Leyuan organization: Wuxi Oncology Institute, the Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China – sequence: 14 givenname: Yugang surname: Wang fullname: Wang, Yugang organization: Department of Urology, University of Michigan Comprehensive Cancer Center, Ann Arbor, Michigan – sequence: 15 givenname: Jian surname: Yu fullname: Yu, Jian organization: State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Shanghai Jiao Tong University School of Medicine, Shanghai, China – sequence: 16 givenname: Xiang surname: Du fullname: Du, Xiang organization: Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai, China – sequence: 17 givenname: Dong surname: Hua fullname: Hua, Dong organization: Wuxi Oncology Institute, the Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China – sequence: 18 givenname: Zhaohui surname: Huang fullname: Huang, Zhaohui email: hzhwxsy@126.com organization: Wuxi Oncology Institute, the Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China. hzhwxsy@126.com |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25294901$$D View this record in MEDLINE/PubMed |
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| Snippet | miR-204-5p was found to be downregulated in colorectal cancer tissues in our preliminary microarray analyses. However, the function of miR-204-5p in colorectal... |
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| SubjectTerms | Animals Base Sequence Binding Sites Cell Line, Tumor Cell Movement - genetics Cell Proliferation Cell Transformation, Neoplastic - genetics Colorectal Neoplasms - drug therapy Colorectal Neoplasms - genetics Colorectal Neoplasms - mortality Colorectal Neoplasms - pathology Disease Models, Animal DNA Methylation Down-Regulation Drug Resistance, Neoplasm - genetics Gene Expression Regulation, Neoplastic Humans Male Mice MicroRNAs - chemistry MicroRNAs - genetics Prognosis Promoter Regions, Genetic rab GTP-Binding Proteins - chemistry rab GTP-Binding Proteins - genetics RNA Interference Tumor Burden Xenograft Model Antitumor Assays |
| Title | miR-204-5p inhibits proliferation and invasion and enhances chemotherapeutic sensitivity of colorectal cancer cells by downregulating RAB22A |
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