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KIAA0101, a target gene of miR-429, enhances migration and chemoresistance of epithelial ovarian cancer cells

View Article: PubMed Central - PubMed

ABSTRACT

Background: Ovarian cancer is a common type of gynecological malignancies, and is the fifth leading cause of cancer-related death in women in the United States. MiR-429 and KIAA0101 have been found to be involved in several human malignancies, respectively. However, the role of miR-429 and KIAA0101, and the correlation between them during development of epithelial ovarian cancer (EOC) remain to be investigated.

Methods: The expression of KIAA0101 in EOC tissues and cells was measured by Quantitative real-time PCR, western blot, and immunochemistry. Cell proliferation assay, colony formation assay, and transwell assay was performed to assess the role of miR-429 and KIAA0101 in regulation of proliferation, migration, and chemoresistance of EOC cells. Luciferase assay was used to test the Wnt/β-catenin signaling activity in response to depletion of KIAA0101 and overexpression of miR-429.

Results: We found that KIAA0101 was upregulated in metastatic EOC tissues, compared to primary EOC tissues, and KIAA0101 was required for the migration activity and chemoresistance of EOC cells by enhancing Wnt/β-catenin signaling. Furthermore, we revealed KIAA0101 is direct target of miR-429. Similar to knockdown of KIAA0101, overexpression of miR-429 reduced invasion and chemoresistance of EOC cells. Co-transfection of KIAA0101 partially abrogates the inhibitory effects on invasion and chemoresistance in EOC cells.

Conclusions: KIAA0101, a target gene of miR-429, was upregulated in the metastatic EOC tissues, and enhanced the migration activity and chemoresistance of EOC cells. Both miR-429 and KIAA0101 may represent the potential therapeutic targets of EOC.

No MeSH data available.


Related in: MedlinePlus

Knockdown of KIAA0101 inhibits ovarian cancer cell migration and invasion. a Expression levels of KIAA0101 was determined by western blot in SKOV3 and COV644 cells transfected with KIAA0101 siRNA (siR-KIAA0101) or control siRNA (siR-Control). b Western blot analysis of E-cadherin and N-cadherin in SKOV3 and COV644 cells transfected with siR-KIAA0101 or siR-Control. c Migration and d Invasion assays in SKOV3 and COV644 cells transfected with siR-KIAA0101 or siR-Control. **p < 0.01, ***p < 0.001 compared with siR-Control transfected cells
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Fig2: Knockdown of KIAA0101 inhibits ovarian cancer cell migration and invasion. a Expression levels of KIAA0101 was determined by western blot in SKOV3 and COV644 cells transfected with KIAA0101 siRNA (siR-KIAA0101) or control siRNA (siR-Control). b Western blot analysis of E-cadherin and N-cadherin in SKOV3 and COV644 cells transfected with siR-KIAA0101 or siR-Control. c Migration and d Invasion assays in SKOV3 and COV644 cells transfected with siR-KIAA0101 or siR-Control. **p < 0.01, ***p < 0.001 compared with siR-Control transfected cells

Mentions: Next, we sought to determine whether downregulation of KIAA0101 expression could affect the metastasis of EOC cells. We transfected KIAA0101 siRNA or control siRNA into SKOV3 and COV644 cells, and confirmed the downregulated expression of KIAA0101 in SKOV3 and COV644 cells after 48 h (Fig. 2a). We performed western blot to assess the expression of EMT markers, E-cadherin and N-cadherin. As shown in Fig. 2b, knockdown of KIAA0101 significantly increased E-cadherin and decreased N-cadherin expression. Furthermore, we discovered that in both cell lines, knockdown of KIAA0101 resulted in a significantly decrease in migration and invasion compared to those transfected with control siRNA, as determined by Transwell assays (Fig. 2c, d). Collectively, these results indicate that KIAA0101 may be required for the metastatic ability of EOC cells.Fig. 2


KIAA0101, a target gene of miR-429, enhances migration and chemoresistance of epithelial ovarian cancer cells
Knockdown of KIAA0101 inhibits ovarian cancer cell migration and invasion. a Expression levels of KIAA0101 was determined by western blot in SKOV3 and COV644 cells transfected with KIAA0101 siRNA (siR-KIAA0101) or control siRNA (siR-Control). b Western blot analysis of E-cadherin and N-cadherin in SKOV3 and COV644 cells transfected with siR-KIAA0101 or siR-Control. c Migration and d Invasion assays in SKOV3 and COV644 cells transfected with siR-KIAA0101 or siR-Control. **p < 0.01, ***p < 0.001 compared with siR-Control transfected cells
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC5037619&req=5

Fig2: Knockdown of KIAA0101 inhibits ovarian cancer cell migration and invasion. a Expression levels of KIAA0101 was determined by western blot in SKOV3 and COV644 cells transfected with KIAA0101 siRNA (siR-KIAA0101) or control siRNA (siR-Control). b Western blot analysis of E-cadherin and N-cadherin in SKOV3 and COV644 cells transfected with siR-KIAA0101 or siR-Control. c Migration and d Invasion assays in SKOV3 and COV644 cells transfected with siR-KIAA0101 or siR-Control. **p < 0.01, ***p < 0.001 compared with siR-Control transfected cells
Mentions: Next, we sought to determine whether downregulation of KIAA0101 expression could affect the metastasis of EOC cells. We transfected KIAA0101 siRNA or control siRNA into SKOV3 and COV644 cells, and confirmed the downregulated expression of KIAA0101 in SKOV3 and COV644 cells after 48 h (Fig. 2a). We performed western blot to assess the expression of EMT markers, E-cadherin and N-cadherin. As shown in Fig. 2b, knockdown of KIAA0101 significantly increased E-cadherin and decreased N-cadherin expression. Furthermore, we discovered that in both cell lines, knockdown of KIAA0101 resulted in a significantly decrease in migration and invasion compared to those transfected with control siRNA, as determined by Transwell assays (Fig. 2c, d). Collectively, these results indicate that KIAA0101 may be required for the metastatic ability of EOC cells.Fig. 2

View Article: PubMed Central - PubMed

ABSTRACT

Background: Ovarian cancer is a common type of gynecological malignancies, and is the fifth leading cause of cancer-related death in women in the United States. MiR-429 and KIAA0101 have been found to be involved in several human malignancies, respectively. However, the role of miR-429 and KIAA0101, and the correlation between them during development of epithelial ovarian cancer (EOC) remain to be investigated.

Methods: The expression of KIAA0101 in EOC tissues and cells was measured by Quantitative real-time PCR, western blot, and immunochemistry. Cell proliferation assay, colony formation assay, and transwell assay was performed to assess the role of miR-429 and KIAA0101 in regulation of proliferation, migration, and chemoresistance of EOC cells. Luciferase assay was used to test the Wnt/&beta;-catenin signaling activity in response to depletion of KIAA0101 and overexpression of miR-429.

Results: We found that KIAA0101 was upregulated in metastatic EOC tissues, compared to primary EOC tissues, and KIAA0101 was required for the migration activity and chemoresistance of EOC cells by enhancing Wnt/&beta;-catenin signaling. Furthermore, we revealed KIAA0101 is direct target of miR-429. Similar to knockdown of KIAA0101, overexpression of miR-429 reduced invasion and chemoresistance of EOC cells. Co-transfection of KIAA0101 partially abrogates the inhibitory effects on invasion and chemoresistance in EOC cells.

Conclusions: KIAA0101, a target gene of miR-429, was upregulated in the metastatic EOC tissues, and enhanced the migration activity and chemoresistance of EOC cells. Both miR-429 and KIAA0101 may represent the potential therapeutic targets of EOC.

No MeSH data available.


Related in: MedlinePlus