scholarly journals Lactucin induces potent anti-cancer effects in HL-60 human leukemia cancer cells by inducing apoptosis and sub-G1 cell cycle arrest

2016 ◽  
Vol 11 (2) ◽  
pp. 478 ◽  
Author(s):  
Fu-Hua Zhang ◽  
Yu-Ling Yan ◽  
Ying Wang ◽  
Zhen Liu
Keyword(s):  
Cell Cycle ◽  
Flow Cytometry ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Phase Contrast ◽  
Human Leukemia ◽  
Apoptotic Cells ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest ◽  
Apoptotic Effects

<p class="Abstract">The main purpose of the present study was to examine the antitumor and apoptotic effects of lactucin in HL-60 human leukemia cancer cells. MTT assay was used to examine the cytotoxic effects of lactucin while as phase contrast, fluorescence and transmission electron microscopy techniques were used to evaluate the apoptotic effects of lactucin in these cells. Flow cytometry was used to assess the effects of lactucin on cell cycle phase distribution. The results indicate that lactucin induced potent, time– and dose-dependent antitumor effects. The microscopic techniques showed that lactucin induced characteristic features of apoptosis including cell shrinkage, membrane blebbing, appearance of vacuoles, swelling of mitochondria and endoplasmic reticulum. Viable cells are stained green, early apoptotic cells are stained yellow, while as late apoptotic cells are stained reddish orange. Flow cytometry revealed that lactucin induced sub-G1 cell cycle arrest.</p><p class="Abstract"><strong>Video Clips</strong></p><p class="Abstract">Phase contrast microscopy:  <a href="https://www.youtube.com/v/xrTjOVvlTxQ">1</a>  <a href="https://www.youtube.com/v/GxuMkGnkpSE">2</a>  <a href="https://www.youtube.com/v/SfmdL2-O45Y">3</a>  <a href="https://www.youtube.com/v/7vbJ9HMRTHU">4</a>  <a href="https://www.youtube.com/v/u4aLzmlXF8s">5</a>  <a href="https://www.youtube.com/v/ucl8DjPeV9c">6</a>  <a href="https://www.youtube.com/v/uI932TJVfFY">7</a>  <a href="https://www.youtube.com/v/5sMlUKbKMhc">8</a>  <a href="https://www.youtube.com/v/-tx20gFHYnc">9</a></p><p> </p>

scholarly journals αO-Conotoxin GeXIVA Inhibits the Growth of Breast Cancer Cells via Interaction with α9 Nicotine Acetylcholine Receptors

Marine Drugs ◽  
2020 ◽  
Vol 18 (4) ◽  
pp. 195 ◽  
Author(s):  
Zhihua Sun ◽  
Jiaolin Bao ◽  
Manqi Zhangsun ◽  
Shuai Dong ◽  
Dongting Zhangsun ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Flow Cytometry ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Cell Line ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Cycle Arrest

The α9-containing nicotinic acetylcholine receptor (nAChR) is increasingly emerging as a new tumor target owing to its high expression specificity in breast cancer. αO-Conotoxin GeXIVA is a potent antagonist of α9α10 nAChR. Nevertheless, the anti-tumor effect of GeXIVA on breast cancer cells remains unclear. Cell Counting Kit-8 assay was used to study the cell viability of breast cancer MDA-MD-157 cells and human normal breast epithelial cells, which were exposed to different doses of GeXIVA. Flow cytometry was adopted to detect the cell cycle arrest and apoptosis of GeXIVA in breast cancer cells. Migration ability was analyzed by wound healing assay. Western blot (WB), quantitative real-time PCR (QRT-PCR) and flow cytometry were used to determine expression of α9-nAChR. Stable MDA-MB-157 breast cancer cell line, with the α9-nAChR subunit knocked out (KO), was established using the CRISPR/Cas9 technique. GeXIVA was able to significantly inhibit the proliferation and promote apoptosis of breast cancer MDA-MB-157 cells. Furthermore, the proliferation of breast cancer MDA-MB-157 cells was inhibited by GeXIVA, which caused cell cycle arrest through downregulating α9-nAChR. GeXIVA could suppress MDA-MB-157 cell migration as well. This demonstrates that GeXIVA induced a downregulation of α9-nAChR expression, and the growth of MDA-MB-157 α9-nAChR KO cell line was inhibited as well, due to α9-nAChR deletion. GeXIVA inhibits the growth of breast cancer cell MDA-MB-157 cells in vitro and may occur in a mechanism abolishing α9-nAChR.

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