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Silencing cyclin-dependent kinase inhibitor 3 inhibits the migration of breast cancer cell lines.

Deng M, Wang J, Chen Y, Zhang L, Xie G, Liu Q, Zhang T, Yuan P, Liu D - Mol Med Rep (2016)

Bottom Line: The underlying mechanisms were screened by detecting proliferating cell nuclear antigen (PCNA), Ras homolog gene family, member A (RhoA), vimentin, B‑cell lymphoma 2 (Bcl‑2) and Bcl‑2‑associated X protein (Bax) expression.Conversely, Bax expression was increased, as compared with the vehicle control.Possible mechanisms are associated with the regulation of PCNA, Bcl‑2, vimentin, RhoA and Bax expression.

View Article: PubMed Central - PubMed

Affiliation: Department of Breast Surgery, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China.

ABSTRACT
Cyclin-dependent kinase inhibitor 3 (CDKN3) belongs to the dual-specificity protein phosphatase family, which is hypothesized to regulate cell cycle progression in tumor cells. However, whether CDKN3 is a potential therapeutic target for breast cancer remains to be elucidated. The present in vitro study aimed to investigate the potential roles of CDKN3 in breast cancer. Breast cancer cell lines were used to detect CDKN3 expression, and CDKN3 expression was silenced to investigate its role in cell apoptosis, cell cycle arrest and migration. The underlying mechanisms were screened by detecting proliferating cell nuclear antigen (PCNA), Ras homolog gene family, member A (RhoA), vimentin, B‑cell lymphoma 2 (Bcl‑2) and Bcl‑2‑associated X protein (Bax) expression. CDKN3 was highly expressed in MCF‑7 and BT474 cell lines. The silencing of CDKN3 in MCF‑7 and BT474 cell lines promoted cell apoptosis, induced G1 phase cell cycle arrest and inhibited cell migration. The expression levels of PCNA, RhoA, vimentin and Bcl‑2 were downregulated following CDKN3 silencing. Conversely, Bax expression was increased, as compared with the vehicle control. These results suggest that CDKN3 acts as an oncogene during breast cancer progression. The in vitro silencing of CDKN3 promoted apoptosis, induced G1 phase cell cycle arrest and inhibited cell migration. Possible mechanisms are associated with the regulation of PCNA, Bcl‑2, vimentin, RhoA and Bax expression. CDKN3 may therefore be considered a potential target for the treatment of breast cancer.

No MeSH data available.


Related in: MedlinePlus

(A) Cyclin-dependent kinase inhibitor 3 silencing resulted in a G1-phase cell cycle arrest in MCF-7 and BT474 cells. (B) Number of cells in G1 phase was determined. Data are presented as the mean ± standard deviation. *P<0.05; **P<0.01 compared with the control group. siRNA, small interfering RNA.
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f4-mmr-14-02-1523: (A) Cyclin-dependent kinase inhibitor 3 silencing resulted in a G1-phase cell cycle arrest in MCF-7 and BT474 cells. (B) Number of cells in G1 phase was determined. Data are presented as the mean ± standard deviation. *P<0.05; **P<0.01 compared with the control group. siRNA, small interfering RNA.

Mentions: CDKN3 is a cell cycle regulatory protein. In the present study, cell cycle distribution was detected following CDKN3 silencing in MCF-7 and BT474 cell lines. As presented in Fig. 4, the number of cells in G1 phase was significantly increased following CDKN3 silencing in MCF-7 and BT474 cell lines (P<0.01 in MCF-7 cells; P<0.05 in BT474 cells). These results suggest that CDKN3 knockdown results in G1 phase arrest in breast cancer cell lines.


Silencing cyclin-dependent kinase inhibitor 3 inhibits the migration of breast cancer cell lines.

Deng M, Wang J, Chen Y, Zhang L, Xie G, Liu Q, Zhang T, Yuan P, Liu D - Mol Med Rep (2016)

(A) Cyclin-dependent kinase inhibitor 3 silencing resulted in a G1-phase cell cycle arrest in MCF-7 and BT474 cells. (B) Number of cells in G1 phase was determined. Data are presented as the mean ± standard deviation. *P<0.05; **P<0.01 compared with the control group. siRNA, small interfering RNA.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4940103&req=5

f4-mmr-14-02-1523: (A) Cyclin-dependent kinase inhibitor 3 silencing resulted in a G1-phase cell cycle arrest in MCF-7 and BT474 cells. (B) Number of cells in G1 phase was determined. Data are presented as the mean ± standard deviation. *P<0.05; **P<0.01 compared with the control group. siRNA, small interfering RNA.
Mentions: CDKN3 is a cell cycle regulatory protein. In the present study, cell cycle distribution was detected following CDKN3 silencing in MCF-7 and BT474 cell lines. As presented in Fig. 4, the number of cells in G1 phase was significantly increased following CDKN3 silencing in MCF-7 and BT474 cell lines (P<0.01 in MCF-7 cells; P<0.05 in BT474 cells). These results suggest that CDKN3 knockdown results in G1 phase arrest in breast cancer cell lines.

Bottom Line: The underlying mechanisms were screened by detecting proliferating cell nuclear antigen (PCNA), Ras homolog gene family, member A (RhoA), vimentin, B‑cell lymphoma 2 (Bcl‑2) and Bcl‑2‑associated X protein (Bax) expression.Conversely, Bax expression was increased, as compared with the vehicle control.Possible mechanisms are associated with the regulation of PCNA, Bcl‑2, vimentin, RhoA and Bax expression.

View Article: PubMed Central - PubMed

Affiliation: Department of Breast Surgery, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China.

ABSTRACT
Cyclin-dependent kinase inhibitor 3 (CDKN3) belongs to the dual-specificity protein phosphatase family, which is hypothesized to regulate cell cycle progression in tumor cells. However, whether CDKN3 is a potential therapeutic target for breast cancer remains to be elucidated. The present in vitro study aimed to investigate the potential roles of CDKN3 in breast cancer. Breast cancer cell lines were used to detect CDKN3 expression, and CDKN3 expression was silenced to investigate its role in cell apoptosis, cell cycle arrest and migration. The underlying mechanisms were screened by detecting proliferating cell nuclear antigen (PCNA), Ras homolog gene family, member A (RhoA), vimentin, B‑cell lymphoma 2 (Bcl‑2) and Bcl‑2‑associated X protein (Bax) expression. CDKN3 was highly expressed in MCF‑7 and BT474 cell lines. The silencing of CDKN3 in MCF‑7 and BT474 cell lines promoted cell apoptosis, induced G1 phase cell cycle arrest and inhibited cell migration. The expression levels of PCNA, RhoA, vimentin and Bcl‑2 were downregulated following CDKN3 silencing. Conversely, Bax expression was increased, as compared with the vehicle control. These results suggest that CDKN3 acts as an oncogene during breast cancer progression. The in vitro silencing of CDKN3 promoted apoptosis, induced G1 phase cell cycle arrest and inhibited cell migration. Possible mechanisms are associated with the regulation of PCNA, Bcl‑2, vimentin, RhoA and Bax expression. CDKN3 may therefore be considered a potential target for the treatment of breast cancer.

No MeSH data available.


Related in: MedlinePlus