OBJECTIVE: Long non-coding RNA (LncRNA) CCAT2 plays an important role in tumorigenesis, tumor growth and metastasis. In this study, we reported that long noncoding RNA CCAT2 (LncRNA CCAT2) could regulate TGF-β signaling pathway in breast cancer. PATIENTS AND METHODS: The relative mRNA expression level of CCAT2 in adjacent non-cancerous and breast cancer tissues without or with metastasis were analyzed by quantitative Real-time polymerase chain reaction (qRT-PCR). The mRNA expression levels of CCAT2 in breast cancer cell lines were analyzed by qRT-PCR. Proliferation, invasion and migration of breast cancer cells were detected after infected with si-NC or si-CCAT2. Flow cytometry analysis was used to detect the cell cycle distribution and apoptosis rate in breast cancer cells after infected with si-NC or si-CCAT2. The relative protein expression level of TGF-β, Smad2 and α-SMA in breast cancer cells after infected with si-NC or si-CCAT2 were analyzed by Western blot. RESULTS: The relative mRNA expression level of CCAT2 in breast cancer tissues was significantly increased compared with adjacent non-cancerous tissues. The expression level of CCAT2 in breast cancer without metastasis was decreased compared with breast cancer metastasis. Meanwhile, down-regulation of CCAT2 inhibited the proliferation, invasion and migration in breast cancer cells. Furthermore, down-regulation of CCAT2 caused breast cancer cells cycle arrested in G0/G1 phase and promoted cell apoptosis. Down-regulation of CCAT2 significantly down-regulated the protein expression levels of TGF-β, Smad2 and α-SMA in breast cancer cells. CONCLUSIONS: CCAT2 was highly expressed in breast cancer. Down-regulation of CCAT2 inhibited the proliferation, invasion and migration and promoted cell apoptosis in breast cancer cells by regulating TGF-β signaling pathway.
OBJECTIVE: Long non-coding RNA (LncRNA) CCAT2 plays an important role in tumorigenesis, tumor growth and metastasis. In this study, we reported that long noncoding RNA CCAT2 (LncRNA CCAT2) could regulate TGF-β signaling pathway in breast cancer. PATIENTS AND METHODS: The relative mRNA expression level of CCAT2 in adjacent non-cancerous and breast cancer tissues without or with metastasis were analyzed by quantitative Real-time polymerase chain reaction (qRT-PCR). The mRNA expression levels of CCAT2 in breast cancer cell lines were analyzed by qRT-PCR. Proliferation, invasion and migration of breast cancer cells were detected after infected with si-NC or si-CCAT2. Flow cytometry analysis was used to detect the cell cycle distribution and apoptosis rate in breast cancer cells after infected with si-NC or si-CCAT2. The relative protein expression level of TGF-β, Smad2 and α-SMA in breast cancer cells after infected with si-NC or si-CCAT2 were analyzed by Western blot. RESULTS: The relative mRNA expression level of CCAT2 in breast cancer tissues was significantly increased compared with adjacent non-cancerous tissues. The expression level of CCAT2 in breast cancer without metastasis was decreased compared with breast cancer metastasis. Meanwhile, down-regulation of CCAT2 inhibited the proliferation, invasion and migration in breast cancer cells. Furthermore, down-regulation of CCAT2 caused breast cancer cells cycle arrested in G0/G1 phase and promoted cell apoptosis. Down-regulation of CCAT2 significantly down-regulated the protein expression levels of TGF-β, Smad2 and α-SMA in breast cancer cells. CONCLUSIONS:CCAT2 was highly expressed in breast cancer. Down-regulation of CCAT2 inhibited the proliferation, invasion and migration and promoted cell apoptosis in breast cancer cells by regulating TGF-β signaling pathway.