Long noncoding RNA PCAT‐1 knockdown prevents the development of ovarian cancer cells via microRNA‐124‐3p
Long noncoding RNA prostate cancer‐associated transcript 1 (PCAT‐1) is overexpressed in human malignancies and its silence abates the exaggeration of cancers. Whereas, the activity of PCAT‐1 silence in ovarian cancer (OC) remains elusive. Here, our study was designed to corroborate the function of P...
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| Veröffentlicht in: | Journal of cellular biochemistry Jg. 121; H. 2; S. 1963 - 1972 |
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| Abstract | Long noncoding RNA prostate cancer‐associated transcript 1 (PCAT‐1) is overexpressed in human malignancies and its silence abates the exaggeration of cancers. Whereas, the activity of PCAT‐1 silence in ovarian cancer (OC) remains elusive. Here, our study was designed to corroborate the function of PCAT‐1 silence in cellular activities and the molecular mechanisms. PCAT‐1 in human ovarian tumor tissue specimens and cell lines (A2780 and SKOV3) were quantified by real‐time quantitative reverse polymerase chain reaction (qRT‐PCR). Reinforced silence of PCAT‐1 and microRNA (miR)‐124‐3p was established by transfection and identified by qRT‐PCR. The viability, apoptosis as well as migration and invasion were examined. Western blot was exploited for analysis of proteins involved in proliferation, apoptosis, migration and invasion, and signaling transduction. OC tissues showed the accumulation of PCAT‐1. Silencing PCAT‐1 caused the impediment of proliferation, migration, and invasion with the increase in apoptosis. PCAT‐1 knockdown repressed the expression of cyclin D1, CDK6, p53, Bax, cleaved caspase‐3, metallopeptidases, and vimentin with the restoration of miR‐124‐3p. However, the roles of PCAT‐1 silence were weakened in the absence of miR‐124‐3p. PCAT‐1 silence caused decrease in Wnt3a, β‐catenin, and phosphorylation of protein kinase B and mechanistic target of rapamycin was abolished by miR‐124‐3p inhibitor. The tumor‐suppressive role of PCAT‐1 silence was mediated by miR‐124‐3p.
Prostate cancer‐associated transcript 1 (PCAT‐1) is overexpressed in human ovarian tumor tissue specimens; PCAT‐1 silence represses the growth of ovarian cancer cells dependent on microRNA (miR)‐124‐3p; Wnt and protein kinase B/AKT/mechanistic target of rapamycin pathways are blocked by PCAT‐1 silence‐induced miR‐124‐3p. |
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| AbstractList | Long noncoding RNA prostate cancer-associated transcript 1 (PCAT-1) is overexpressed in human malignancies and its silence abates the exaggeration of cancers. Whereas, the activity of PCAT-1 silence in ovarian cancer (OC) remains elusive. Here, our study was designed to corroborate the function of PCAT-1 silence in cellular activities and the molecular mechanisms. PCAT-1 in human ovarian tumor tissue specimens and cell lines (A2780 and SKOV3) were quantified by real-time quantitative reverse polymerase chain reaction (qRT-PCR). Reinforced silence of PCAT-1 and microRNA (miR)-124-3p was established by transfection and identified by qRT-PCR. The viability, apoptosis as well as migration and invasion were examined. Western blot was exploited for analysis of proteins involved in proliferation, apoptosis, migration and invasion, and signaling transduction. OC tissues showed the accumulation of PCAT-1. Silencing PCAT-1 caused the impediment of proliferation, migration, and invasion with the increase in apoptosis. PCAT-1 knockdown repressed the expression of cyclin D1, CDK6, p53, Bax, cleaved caspase-3, metallopeptidases, and vimentin with the restoration of miR-124-3p. However, the roles of PCAT-1 silence were weakened in the absence of miR-124-3p. PCAT-1 silence caused decrease in Wnt3a, β-catenin, and phosphorylation of protein kinase B and mechanistic target of rapamycin was abolished by miR-124-3p inhibitor. The tumor-suppressive role of PCAT-1 silence was mediated by miR-124-3p. Long noncoding RNA prostate cancer‐associated transcript 1 (PCAT‐1) is overexpressed in human malignancies and its silence abates the exaggeration of cancers. Whereas, the activity of PCAT‐1 silence in ovarian cancer (OC) remains elusive. Here, our study was designed to corroborate the function of PCAT‐1 silence in cellular activities and the molecular mechanisms. PCAT‐1 in human ovarian tumor tissue specimens and cell lines (A2780 and SKOV3) were quantified by real‐time quantitative reverse polymerase chain reaction (qRT‐PCR). Reinforced silence of PCAT‐1 and microRNA (miR)‐124‐3p was established by transfection and identified by qRT‐PCR. The viability, apoptosis as well as migration and invasion were examined. Western blot was exploited for analysis of proteins involved in proliferation, apoptosis, migration and invasion, and signaling transduction. OC tissues showed the accumulation of PCAT‐1. Silencing PCAT‐1 caused the impediment of proliferation, migration, and invasion with the increase in apoptosis. PCAT‐1 knockdown repressed the expression of cyclin D1, CDK6, p53, Bax, cleaved caspase‐3, metallopeptidases, and vimentin with the restoration of miR‐124‐3p. However, the roles of PCAT‐1 silence were weakened in the absence of miR‐124‐3p. PCAT‐1 silence caused decrease in Wnt3a, β‐catenin, and phosphorylation of protein kinase B and mechanistic target of rapamycin was abolished by miR‐124‐3p inhibitor. The tumor‐suppressive role of PCAT‐1 silence was mediated by miR‐124‐3p. Prostate cancer‐associated transcript 1 (PCAT‐1) is overexpressed in human ovarian tumor tissue specimens; PCAT‐1 silence represses the growth of ovarian cancer cells dependent on microRNA (miR)‐124‐3p; Wnt and protein kinase B/AKT/mechanistic target of rapamycin pathways are blocked by PCAT‐1 silence‐induced miR‐124‐3p. Long noncoding RNA prostate cancer-associated transcript 1 (PCAT-1) is overexpressed in human malignancies and its silence abates the exaggeration of cancers. Whereas, the activity of PCAT-1 silence in ovarian cancer (OC) remains elusive. Here, our study was designed to corroborate the function of PCAT-1 silence in cellular activities and the molecular mechanisms. PCAT-1 in human ovarian tumor tissue specimens and cell lines (A2780 and SKOV3) were quantified by real-time quantitative reverse polymerase chain reaction (qRT-PCR). Reinforced silence of PCAT-1 and microRNA (miR)-124-3p was established by transfection and identified by qRT-PCR. The viability, apoptosis as well as migration and invasion were examined. Western blot was exploited for analysis of proteins involved in proliferation, apoptosis, migration and invasion, and signaling transduction. OC tissues showed the accumulation of PCAT-1. Silencing PCAT-1 caused the impediment of proliferation, migration, and invasion with the increase in apoptosis. PCAT-1 knockdown repressed the expression of cyclin D1, CDK6, p53, Bax, cleaved caspase-3, metallopeptidases, and vimentin with the restoration of miR-124-3p. However, the roles of PCAT-1 silence were weakened in the absence of miR-124-3p. PCAT-1 silence caused decrease in Wnt3a, β-catenin, and phosphorylation of protein kinase B and mechanistic target of rapamycin was abolished by miR-124-3p inhibitor. The tumor-suppressive role of PCAT-1 silence was mediated by miR-124-3p.Long noncoding RNA prostate cancer-associated transcript 1 (PCAT-1) is overexpressed in human malignancies and its silence abates the exaggeration of cancers. Whereas, the activity of PCAT-1 silence in ovarian cancer (OC) remains elusive. Here, our study was designed to corroborate the function of PCAT-1 silence in cellular activities and the molecular mechanisms. PCAT-1 in human ovarian tumor tissue specimens and cell lines (A2780 and SKOV3) were quantified by real-time quantitative reverse polymerase chain reaction (qRT-PCR). Reinforced silence of PCAT-1 and microRNA (miR)-124-3p was established by transfection and identified by qRT-PCR. The viability, apoptosis as well as migration and invasion were examined. Western blot was exploited for analysis of proteins involved in proliferation, apoptosis, migration and invasion, and signaling transduction. OC tissues showed the accumulation of PCAT-1. Silencing PCAT-1 caused the impediment of proliferation, migration, and invasion with the increase in apoptosis. PCAT-1 knockdown repressed the expression of cyclin D1, CDK6, p53, Bax, cleaved caspase-3, metallopeptidases, and vimentin with the restoration of miR-124-3p. However, the roles of PCAT-1 silence were weakened in the absence of miR-124-3p. PCAT-1 silence caused decrease in Wnt3a, β-catenin, and phosphorylation of protein kinase B and mechanistic target of rapamycin was abolished by miR-124-3p inhibitor. The tumor-suppressive role of PCAT-1 silence was mediated by miR-124-3p. |
| Author | Chu, Guoyan Min, Fengying |
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| Snippet | Long noncoding RNA prostate cancer‐associated transcript 1 (PCAT‐1) is overexpressed in human malignancies and its silence abates the exaggeration of cancers.... Long noncoding RNA prostate cancer-associated transcript 1 (PCAT-1) is overexpressed in human malignancies and its silence abates the exaggeration of cancers.... |
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| SubjectTerms | Apoptosis Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Cell Movement Cell Proliferation Female Gene Expression Regulation, Neoplastic Humans MicroRNAs - genetics miR‐124‐3p ovarian cancer Ovarian Neoplasms - genetics Ovarian Neoplasms - metabolism Ovarian Neoplasms - pathology PCAT‐1 RNA, Long Noncoding - genetics Tumor Cells, Cultured |
| Title | Long noncoding RNA PCAT‐1 knockdown prevents the development of ovarian cancer cells via microRNA‐124‐3p |
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