Limits...
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 enhances ovarian cancer cell chemosensitivity. a SKOV3 and COV644 cells were cultured in complete medium with Cisplatin (8 µM) for 24 h, then medium was changed without Cisplatin for 48 h. The KIAA0101 expression were examined by qRT-PCR at different time points indicated. b MTT cell growth rate and c colony formation assays were performed in KIAA0101 knockdown SKOV3 and COV644 cells treated with different concentration of Cisplatin indicated. *p < 0.05 compared with siR-Control transfected cells
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

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

Fig3: Knockdown of KIAA0101 enhances ovarian cancer cell chemosensitivity. a SKOV3 and COV644 cells were cultured in complete medium with Cisplatin (8 µM) for 24 h, then medium was changed without Cisplatin for 48 h. The KIAA0101 expression were examined by qRT-PCR at different time points indicated. b MTT cell growth rate and c colony formation assays were performed in KIAA0101 knockdown SKOV3 and COV644 cells treated with different concentration of Cisplatin indicated. *p < 0.05 compared with siR-Control transfected cells

Mentions: KIAA0101 has been reported involving in drug resistance in esophageal and hepatocellular cancers [19, 24]. To explore whether KIAA0101 regulates EOC chemoresistance, we first treated SKOV3 and COV644 cells with 8 µM Cisplatin for 24 h and then changed to complete medium without Cisplatin for 48 h. KIAA0101 expression were examined at different time points. The results revealed that KIAA0101 was significantly upregulated after 6 h of Cisplatin treatment (Fig. 3a). We next treated EOC cells with different concentration of Cisplatin and performed MTT assays to examine cell growth rate. As shown in Fig. 3b, knockdown of KIAA0101 resulted in EOC cells more sensitive to Cisplatin treatment.Fig. 3


KIAA0101, a target gene of miR-429, enhances migration and chemoresistance of epithelial ovarian cancer cells
Knockdown of KIAA0101 enhances ovarian cancer cell chemosensitivity. a SKOV3 and COV644 cells were cultured in complete medium with Cisplatin (8 µM) for 24 h, then medium was changed without Cisplatin for 48 h. The KIAA0101 expression were examined by qRT-PCR at different time points indicated. b MTT cell growth rate and c colony formation assays were performed in KIAA0101 knockdown SKOV3 and COV644 cells treated with different concentration of Cisplatin indicated. *p < 0.05 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

Fig3: Knockdown of KIAA0101 enhances ovarian cancer cell chemosensitivity. a SKOV3 and COV644 cells were cultured in complete medium with Cisplatin (8 µM) for 24 h, then medium was changed without Cisplatin for 48 h. The KIAA0101 expression were examined by qRT-PCR at different time points indicated. b MTT cell growth rate and c colony formation assays were performed in KIAA0101 knockdown SKOV3 and COV644 cells treated with different concentration of Cisplatin indicated. *p < 0.05 compared with siR-Control transfected cells
Mentions: KIAA0101 has been reported involving in drug resistance in esophageal and hepatocellular cancers [19, 24]. To explore whether KIAA0101 regulates EOC chemoresistance, we first treated SKOV3 and COV644 cells with 8 µM Cisplatin for 24 h and then changed to complete medium without Cisplatin for 48 h. KIAA0101 expression were examined at different time points. The results revealed that KIAA0101 was significantly upregulated after 6 h of Cisplatin treatment (Fig. 3a). We next treated EOC cells with different concentration of Cisplatin and performed MTT assays to examine cell growth rate. As shown in Fig. 3b, knockdown of KIAA0101 resulted in EOC cells more sensitive to Cisplatin treatment.Fig. 3

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