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The mechanism and clinical significance of long non-coding RNA plasmacytoma variant translocation gene 1 in regulating the differentiation, proliferation, invasion and metastasis of breast cancer cells through target genes / 中国医师进修杂志
Chinese Journal of Postgraduates of Medicine ; (36): 637-643, 2021.
Article in Chinese | WPRIM | ID: wpr-908652
ABSTRACT

Objective:

To analyze the mechanism and significance of long non-coding RNA (LncRNA) plasmacytoma variant translocation gene 1 (PVT1) in regulating the proliferation, differentiation, invasion and metastasis of breast cancer cells through the target gene.

Methods:

From January 2018 to December 2019, the expression levels of LncRNA PVT1 and microRNA (miR)-1207-5p in breast cancer cell line MCF-7 and normal breast epithelial cell line MCF-10A were detected by real-time fluorescence quantitative polymerase chain reaction (qRT-PCR). The human breast cancer cell line MCF-7 was transfected with PVT1 overexpression vector plasmid, PVT1 silencing lentivirus plasmid and negative control plasmid, and the expression levels of PVT1 and miR-1207-5p after transfection were detected. The activities of proliferation differentiation, metastasis and invasion in transfected breast cancer cells were detected by CCK-8 method, cell scratch test and Transwell invasion experiment. The expression levels of signal transducer and activator of transcription 6 (STAT6) and P21 mRNA/protein after transfection miR-1207-5p were detected by qRT-PCR and Western blotting method.

Results:

The expression levels of PVT1 and miR-1207-5p in breast cancer cells were significantly higher than those in normal breast epithelial cells (1.271 ± 0.305 vs. 0.023 ± 0.006 and 1.679 ± 0.347 vs. 0.031 ± 0.009), and there were statistical differences ( P<0.01). The expression levels of PVT1 and miR-1207-5p in breast cancer cells after transfection PVT1 overexpression vector plasmid were significantly higher than those in breast cancer cells after transfection negative control plasmid and PVT1 silencing lentivirus plasmid (2.357 ± 0.271 vs. 1.000 ± 0.000 and 0.103 ± 0.021, 3.265±0.375 vs. 1.000 ± 0.000 and 0.265 ± 0.024), the indexes in breast cancer cells after transfection negative control plasmid were significantly higher than those in breast cancer cells after transfection PVT1 silencing lentivirus plasmid, and there were statistical differences ( P<0.05). The proliferation activity in breast cancer cells 48, 72, 96 and 168 h after transfected with PVT1 overexpression vector plasmid was significantly higher than that in breast cancer cells transfected with negative control plasmid and PVT1 silencing lentivirus plasmid, proliferation activity in breast cancer cells transfected with negative control plasmid was significantly higher than that in breast cancer cells transfected with PVT1 silencing lentivirus plasmid, and there were statistical differences ( P<0.05). The metastasis activity and invasion activity in breast cancer cells 24 h after transfected with PVT1 overexpression vector plasmid were significantly higher than those in breast cancer cells transfected with negative control plasmid and PVT1 silencing lentivirus plasmid, the metastasis activity in breast cancer cells transfected negative control plasmid was significantly higher than that in breast cancer cells transfected PVT1 silencing lentivirus plasmid, and there were statistical differences ( P<0.05). The STAT6 and P21 mRNA in transfection miR-1207-5p overexpression group were significantly lower than those in transfection mimic group (0.476 ± 0.102 vs. 1.000 ± 0.000 and 0.429 ± 0.097 vs. 1.132 ± 0.236), and there were statistical differences ( P<0.01); the STAT6 and P21 protein in miR-1207-5p overexpression group was significantly lower than that in mimic group (0.396 ± 0.104 vs. 1.062 ± 0.002 and 0.434 ± 0.067 vs. 1.141 ± 0.218), and there were statistical differences ( P<0.01).

Conclusions:

LncRNA PVT1 may be a regulated host gene of miR-1207-5p, which synergistically affects the proliferation, differentiation, invasion and metastasis of breast cancer cells through the regulation of target gene STAT6. Inhibiting the transcription of this gene may be a new research direction for breast cancer treatment.

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Postgraduates of Medicine Year: 2021 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Postgraduates of Medicine Year: 2021 Type: Article