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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) CDKN3 was highly expressed in the MCF-7 and BT474 cell lines. siRNA was used to silence CDKN3 expression in (B) MCF-7 and (C) BT474 cells. (D) CDKN3 protein expression levels relative to GAPDH. Data are presented as the mean ± standard deviation. *P<0.05; **P<0.01; ***P<0.001 vs. the control group. CDKN3, cyclin-dependent kinase inhibitor 3; siRNA, small interfering RNA; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.
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f1-mmr-14-02-1523: (A) CDKN3 was highly expressed in the MCF-7 and BT474 cell lines. siRNA was used to silence CDKN3 expression in (B) MCF-7 and (C) BT474 cells. (D) CDKN3 protein expression levels relative to GAPDH. Data are presented as the mean ± standard deviation. *P<0.05; **P<0.01; ***P<0.001 vs. the control group. CDKN3, cyclin-dependent kinase inhibitor 3; siRNA, small interfering RNA; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.

Mentions: To investigate the function of CDKN3 expression in tumor growth, CDKN3 expression levels were detected in a number of breast cancer cell lines, including MCF-7, ZR-75-30, T47-D, MDA-MB-231 and BT474. As demonstrated by western blot analysis, CDKN3 was highly expressed in the MCF-7 and BT474 cell lines (Fig. 1A). In subsequent experiments, siRNA was used to knockdown the expression of CDKN3 in MCF-7 and BT474 cell lines. Three siRNA sequences were designed and the optimal knockdown effect was observed using the siRNA3 sequence. As presented in Fig. 1B–D, siRNA significantly decreased the CDKN3 expression levels in the MCF-7 and BT474 cell lines compared with the control (P<0.001). However, the vehicle sequence did not affect CDKN3 expression. These results suggest that CDKN3 is overexpressed in certain types of breast cancer cell lines and that siRNA is an effective approach to knockdown the expression levels of CDKN3.


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) CDKN3 was highly expressed in the MCF-7 and BT474 cell lines. siRNA was used to silence CDKN3 expression in (B) MCF-7 and (C) BT474 cells. (D) CDKN3 protein expression levels relative to GAPDH. Data are presented as the mean ± standard deviation. *P<0.05; **P<0.01; ***P<0.001 vs. the control group. CDKN3, cyclin-dependent kinase inhibitor 3; siRNA, small interfering RNA; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f1-mmr-14-02-1523: (A) CDKN3 was highly expressed in the MCF-7 and BT474 cell lines. siRNA was used to silence CDKN3 expression in (B) MCF-7 and (C) BT474 cells. (D) CDKN3 protein expression levels relative to GAPDH. Data are presented as the mean ± standard deviation. *P<0.05; **P<0.01; ***P<0.001 vs. the control group. CDKN3, cyclin-dependent kinase inhibitor 3; siRNA, small interfering RNA; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.
Mentions: To investigate the function of CDKN3 expression in tumor growth, CDKN3 expression levels were detected in a number of breast cancer cell lines, including MCF-7, ZR-75-30, T47-D, MDA-MB-231 and BT474. As demonstrated by western blot analysis, CDKN3 was highly expressed in the MCF-7 and BT474 cell lines (Fig. 1A). In subsequent experiments, siRNA was used to knockdown the expression of CDKN3 in MCF-7 and BT474 cell lines. Three siRNA sequences were designed and the optimal knockdown effect was observed using the siRNA3 sequence. As presented in Fig. 1B–D, siRNA significantly decreased the CDKN3 expression levels in the MCF-7 and BT474 cell lines compared with the control (P<0.001). However, the vehicle sequence did not affect CDKN3 expression. These results suggest that CDKN3 is overexpressed in certain types of breast cancer cell lines and that siRNA is an effective approach to knockdown the expression levels of CDKN3.

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