In Vitro Cellular & Developmental Biology - Animal

LINC00319 promotes migration, invasion and epithelial-mesenchymal transition process in cervical cancer by regulating miR-3127-5p/RPP25 axis

Cervical cancer is among the most prevalent malignancies for women. An increasing number of evidences have been proved that long non-coding RNAs (lncRNAs) play significant role in the initiation and progression of cervical cancer. However, the function of long intergenic non-protein coding RNA 319 (LINC00319) in cervical cancer still remains vague. In this study, our purpose was to investigate the effects of LINC00319 on cell migration, invasion and epithelial-mesenchymal transition (EMT) process in cervical cancer. It confirmed that LINC00319 was highly expressed in tissues and cell lines in cervical cancer. Further, overexpression of LINC00319 accelerates cell migration, invasion and EMT in cervical cancer. Moreover, LINC00319 could bind with miR-3127-5p and negatively regulated its expression. Besides, RPP25 was targeted by miR-3127-5p, and its expression was negatively/positively regulated by miR-3127-5p/LINC00319. Additionally, miR-3127-5p mimics or RPP25 insufficiency could offset the encouraging effects of LINC00319 overexpression on migration, invasion and EMT process in cervical cancer. Generally speaking, LINC00319 promotes migration, invasion and EMT process in cervical cancer by regulating miR-3127-5p/RPP25 axis, which may be conductive to cervical cancer treatment.

Enhanced KRT13 gene expression bestows radiation resistance in squamous cell carcinoma cells

Cancer metastasis and recurrence are potentially lethal. A small number of cancer cell groups called cancer stem cells (CSCs) have both stem cell capacity and cancer-forming ability and are reported to play important roles in cancer metastasis and recurrence. These CSCs are considered to be radiation-resistant (RR). Therefore, understanding the biological effects of radiation on squamous cell carcinoma (SCC) cell lines in vitro and in vivo might be worthwhile to circumvent radiation resistance. Currently, there are no reports on the establishment of RR-SCC cells in serum-free defined culture, which mimics biological mechanisms and prevents instability of using serum in the culture medium. We isolated radiation-resistant strains, designated A431-LDR and A431-HDR, from A431 cells derived from vulval SCC and irradiated them with a total dose of 60 Gy at a low-dose rate (2.2 Gy/d) (RM1000) and a high-dose rate (5 Gy/5.75min) in serum-free defined culture. These cells exhibited high sphere-forming and migration ability in vitro and high tumor-forming ability in nude mice xenografts. Overexpression of KRT13 in A431-RR cells might play a role in its radiation-resistant characteristics. These cells might be useful not only to study cancer stem cells but also to study the circumvention of radiation resistance by novel cancer treatment modalities.

Epigallocatechin gallate inhibits ovarian cancer cell growth and induces cell apoptosis via activation of FOXO3A

Epigallocatechin gallate (EGCG), a bioactive component in tea, displays broad anti-cancer effects. Our study was designed to evaluate the anti-cancer effects of EGCG on ovarian cancer and explored the underlying molecular mechanisms. To evaluate the in vitro inhibitory effects of EGCG against ovarian cancer, MTT assay, colony formation assay, apoptosis assay, and wound healing assay, were performed. Besides, the inhibitory effects of EGCG on tumor growth in the xenograft animal model were evaluated by measuring tumor volume and tumor weight. Moreover, Western blotting and qPCR were used to evaluate the levels of target genes and proteins. Treatment with EGCG inhibited cell migration and cell survival, and promoted cell apoptosis in A2780 and SKOV3 cells. Interestingly, treatment with EGCG inhibited the tumor growth in the xenograft animal model. The mechanistic study revealed that treatment with EGCG induced the activation of FOXO3A and suppressed the expression of c-Myc both in vitro and in vivo. Our findings demonstrate that EGCG suppress ovarian cancer cell growth, which may be due to its regulation on FOXO3A and c-Myc.