In this study, chitosan-assembled zinc oxide nanoparticle (CZNP) was successfully prepared for evaluated for its anticancer efficacy against cervical cancer cells. The CZNP particles were nanosized and spherical in shape. The zinc oxide nanoparticle (ZNP) and CZNP showed significant cytotoxicity in cervical cancer cells in a concentration-dependent manner. Results showed that the enhanced cytotoxicity was mainly attributed to the reactive oxygen species (ROS) generation in the cancer cells. The apoptosis assay further revealed that apoptosis was the main reason behind the cell killing effect of the zinc oxide nanoparticles. The apoptosis was further confirmed by the nuclear chromatin assay. Live dead assay showed increased red fluorescent cell for CZNP treated cancer cells. Overall, metal oxide present in nanoparticulate dimensions will be advantageous in imparting the cytotoxicity to cervical cancer cell.
Paclitaxel is recommended as a first-line chemotherapeutic agent against ovarian cancer, but drug resistance becomes a major limitation of its success clinically. The key molecule or mechanism associated with paclitaxel resistance in ovarian cancer still remains unclear. Sex-determining region Y-box 2 (SOX2) is of vital importance in the regulation of stem cell proliferation and carcinogenesis. The aim of this study was to evaluate the role of SOX2 in ovarian cancer tumorigenesis and paclitaxel resistance. In the present study, the expression of SOX2 was examined by immunohistochemistry (IHC) and real-time PCR in 40 clinical samples and in SKOV3 cells and SKOV3/TAX cells (paclitaxel-resistant human ovarian adenocarcinoma cell line). The effects of SOX2 knockdown on ovarian cancer cell proliferation, migration, and invasion were also studied. The IHC and real-time PCR results showed that the difference of SOX2 expression between ovarian cancer and the adjacent non-tumorous ovarian tissues was statistically significant. Western blot analysis revealed that the PI3K/Akt signaling pathway was inhibited in cells overexpressing SOX2. Western blot analysis showed that the SOX2 protein was overexpressed in paclitaxel-resistant cells and weakly detectable in paclitaxel-sensitive cells. SOX2 silencing significantly potentiated apoptosis induced by paclitaxel in SKOV3-TR with SOX2 knockdown compared to SKOV3-TR transfected with control small interfering RNA (siRNA). Our work indicates SOX2 will become both a rational indicator of ovarian cancer prognosis and a promising target for ovarian cancer gene therapy.
Objective: Long non-coding RNAs (lncRNAs) have been identified as important players in tumorigenesis. LncRNA TMPO antisense RNA 1 (TMPO-AS1) has been shown to be involved in several tumors. However, the functional role and the underlying mechanism of TMPO-AS1 in regulating cervical cancer cell behavior remain unclear. Materials and Methods: Expression of TMPO-AS1, miR-143-3p, and ZEB1 were examined by qRT-PCR and Western blot. Cell proliferation, migration and invasion were evaluated using CCK-8 assay and Transwell migration and invasion assays, respectively. Luciferase reporter assay was performed to investigate the interaction miR-143-3p and TMPO-AS1 or ZEB1. Results: TMPO-AS1 was highly expressed in cervical cancer cells. Furthermore, TMPO-AS1 overexpression significantly promoted C-33A cell proliferation, migration, and invasion. In contrast, TMPO-AS1 silencing inhibited SiHa cell proliferation, migration, and invasion. Mechanistically, TMPO-AS1 acted as a sponge of miR-143-3p to elevate expression of zinc finger E-box binding homeobox 1 (ZEB1), a target of miR-143-3p, and thereby promoted C-33A cell proliferation, migration, and invasion. Further assays showed that TMPO-AS1 knockdown inhibited cervical cancer cell tumorigenesis in vivo. Conclusion: TMPO-AS1 promotes cervical cancer cell proliferation, migration, and invasion by regulating the miR-143-3p/ZEB1 axis.
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