Down-regulation of C35 decreased the cell viability and migration of breast ductal carcinoma cells

Abstract Background Mammary cancer is a common disease affecting female dogs, where approximately 50% of the cases are malignant. There is a subpopulation of cancer cells with stem cell-like features within the tumour microenvironment, which can form in vitro spheres, cell structures that grow in anchor-free conditions. This cell population shows resistance to conventional antitumor treatments explaining in part the recurrence of some type of cancers. It has been previously reported that spheres derived from CF41.Mg canine mammary carcinoma cells exhibit several stemness features. Melatonin has shown antitumor effects on cancer mammary cells; nevertheless, its effects have been poorly evaluated on canine mammary cancer stem-like cells. In this regard, it has described that melatonin decreases the expression of OCT-4 in CMT-U2229 mammary cancer cells, a transcription factor that participates in the modulation of self-renewal and drug resistance in cancer stem-like cells. The aim of this study was to compare the effects of melatonin on viability and migration of canine mammary carcinoma CF41.Mg-spheres, and CF41.Mg-parental cells. CF41.Mg cells were grown in DMEM high-glucose medium containing 10% bovine foetal serum. CF41.Mg-spheres were cultured in ultra-low attachment plates with serum-free DMEM/F12 containing several growth factors. Cell viability (MTS reduction) and migration (transwell) assays were conducted in presence of melatonin (0.01, 0.1 or 1 mM). Results Melatonin decreased cell viability at 1 mM (P < 0.05), with a significant reduction in spheres compared to parental cells at 24 and 48 h (P < 0.05). Cell migration was inhibited in response to non-cytotoxic concentration of melatonin (0.1 mM) (P < 0.05) in spheres and monolayer of cells, no significant differences were detected between both cell subtypes. Conclusions These results indicate that melatonin reduces viability and migration of CF41.Mg cells, where spheres exhibit greater sensitivity to the hormone. Thus, melatonin represents a valuable potential agent against mammary cancer cells, especially cancer stem-like cells.

Download Full-text

Ludartin treatment exhibits promising inhibitory effect on the epithelial ovarian cancer growth and metastasis

Bangladesh Journal of Pharmacology ◽

10.3329/bjp.v11i3.26692 ◽

2016 ◽

Vol 11 (3) ◽

pp. 646

Author(s):

Lin Bai ◽

Hui Wang ◽

Luo-Ying Zhang ◽

Ai-Hua Wang ◽

Jie Bai

Keyword(s):

Ovarian Cancer ◽

Cell Viability ◽

Video Clip ◽

Inhibitory Effect ◽

Carcinoma Cells ◽

Ovarian Cancer Cells ◽

Invasive Potential ◽

Invasion And Migration ◽

Migration Potential ◽

And Migration

In the present study, the effect of ludartin on OVCAR5 ovarian carcinoma cells was investigated. MTT cell assay was used for the analysis of cell viability and wound healing assay for migration potential. Results revealed that ludartin treatment at 10 and 30 µM doses reduced the cell viability from 94 to 38%. The invasive potential was decreased from 62 to 24% with increase in ludartin concentration from 10 to 30 µM. Western blot analysis showed that ludartin treatment reduced the expression of p-FAK in OVCAR5 cells significantly. Ludartin treatment for 48 hours also caused a significant decrease in the expression of MMP-2 and MMP-9 in OVCAR5 cells at a concentration of 30 µM. The metastatic regions were absent in the rats treated with 30 µM/kg doses of ludartin daily for 15 days. Thus, ludartin treatment inhibits the proliferation, invasion and migration of ovarian cancer cells through down-regulation of pFAK and MMPs, therefore can be used for the treatment of ovarian cancer.Video Clip:<a href="https://youtube.com/v/GMpEHXdGSeI">Cell proliferation assay:</a> 2 min 45 sec

Download Full-text

Down-regulation of SOX18 inhibits laryngeal carcinoma cell proliferation, migration, and invasion through JAK2/STAT3 signaling

Bioscience Reports ◽

10.1042/bsr20182480 ◽

2019 ◽

Vol 39 (7) ◽

Cited By ~ 3

Author(s):

Yice Xu ◽

Qingyuan Zhang ◽

Jie Zhou ◽

Zhaolong Li ◽

Junyu Guo ◽

...

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Laryngeal Carcinoma ◽

Carcinoma Cell ◽

Carcinoma Cells ◽

Migration And Invasion ◽

Down Regulation ◽

Invasion And Migration ◽

Stat3 Signaling ◽

And Migration

AbstractLaryngeal carcinoma is one of the most common malignant tumors of the head, neck, and respiratory tract. The aim of the present study is to explore the biological function of SRY-related HMG-box 18 (SOX18) in laryngeal carcinoma cells and study the molecular mechanism involved. Initial findings indicate that the expression of SOX18 was increased in laryngeal carcinoma cell lines and tissues. The effect of SOX18 on laryngeal carcinoma cell proliferation, cell cycle, apoptosis, invasion, and migration was also identified. The results indicated that down-regulation of SOX18 significantly inhibited cell proliferation, migration, and invasion, and induced cell-cycle arrest in G0/G1 phase and apoptosis of laryngeal carcinoma cells. However, overexpression of SOX18 promoted cell proliferation, invasion, and migration, and inhibited cell apoptosis. The expression of cyclin D1, active-caspase-3, N-cadherin, MTA1, MMP-2, and MMP-7 was also regulated by the overexpression of siSOX18 or SOX18. In addition, it was found that SOX18 could also accelerate the phosphorylation of JAK2/STAT3 signaling in laryngeal carcinoma cells. Furthermore, our study indicated that SOX18 could stimulate cell proliferation, migration, and invasion of laryngeal carcinoma cells via regulation of JAK2/STAT3 signaling, which could provide a new strategy for laryngeal carcinoma diagnosis and molecular therapies.

Download Full-text

Down-Regulation of TMPO-AS1 Induces Apoptosis in Lung Carcinoma Cells by Regulating miR-143-3p/CDK1 Axis

Technology in Cancer Research & Treatment ◽

10.1177/1533033820948880 ◽

2021 ◽

Vol 20 ◽

pp. 153303382094888

Author(s):

Qiu Li ◽

Yuan Bian ◽

Qiaolian Li

Keyword(s):

Cell Viability ◽

Cell Apoptosis ◽

Carcinoma Cells ◽

Luciferase Reporter ◽

Down Regulation ◽

Novel Therapy ◽

Lung Carcinoma Cells ◽

Kaplan Meier ◽

Reporter Assays ◽

Related Proteins

Evidence has shown that long non-coding RNAs (lncRNA) play pivotal roles in cancer promotion as well as suppression. But the molecular mechanism of lncRNA TMPO antisense transcript 1 (TMPO-AS1) in lung cancer (LC) remains unclear. This study mainly investigated the effect of TMPO-AS1 in LC treatment. TMPO-AS1 was tested by Kaplan-Meier method. Quantitative real time polymerase chain reaction (qRT-PCR) was employed to assess the expressions of TMPO-AS1, miR-143-3p, and CDK1 respectively in LC tissues and cell lines. TMPO-AS1, miR-143-3p and CDK1 expressions in LC cells were regulated through cell transfection, followed by MTT for cell viability detection. Besides, dual-luciferase reporter assays were performed to verify the interrelated microRNA of TMPO-AS1 and the target of miR-143-3p. Western blot experiments were used to examine the expressions of apoptosis-related proteins, and flow cytometry tested the cell apoptosis in treated cells. TMPO-AS1 and CDK1 were overexpressed in LC tissues and cells, while miR-143-3p level was suppressed. The decrease of TMPO-AS1 led to the increase of miR-143-3p, which further resulted in the reduction of CDK1. Down-regulating TMPO-AS1 reduced LC cell viability, motivated cell apoptosis, as well as promoted the expressions of Bcl and CCND1 and restrained Caspase-3 level, but all these consequences were abrogated by miR-143-3p inhibitor. Simultaneously, siCDK1 could reverse the anti-apoptosis and pro-activity functions of miR-143-3p inhibitor in LC cells. Down-regulation of TMPO-AS1 has the effects of pro-apoptosis in LC by manipulating miR-143-3p/CDK1, which is hopeful to be a novel therapy for LC patients.

Download Full-text