scholarly journals Anti-proliferative and apoptosis-inducing effects of matricin on human non-small cell lung cancer H1299 cells via MAPK pathway activation

2020 ◽  
Vol 18 ◽  
pp. 205873922094233
Author(s):  
Xiaoying Bai ◽  
Wei Wang ◽  
Yan Wang ◽  
Jing Li

Lung cancer in humans is majorly represented by non-small cell lung cancer cells, and there is a constant search for an efficient therapeutic approach. This study aims to find the anti-proliferative and apoptotic effects of matricin on H1299 cells via activation of MAPK pathway. Non-small cell H1299 cells were subjected to viability analysis with MTT assay and anti-proliferation analysis with different concentrations of matricin. Apoptosis was determined with annexin V/propidium iodide (PI) and flow cytometric analysis. Analysis of oxidative stress markers, reduced glutathione, lipid peroxidation (LPO), superoxide dismutase (SOD), and catalase (CAT) activities were done using standard assay kits. Apoptosis enzymes caspase-3, caspase-8, and caspase-9 levels were measured using colorimetric kit analysis. Western blot analysis on apoptotic proteins was performed to determine the involvement of MAPK pathway activation in apoptosis. Matricin significantly ( P < 0.01) exerted anti-proliferative activities on H1299 cells in a dose-dependent manner. Flow cytometric apoptosis analysis showed increasing concentrations of matricin had increased apoptosis ( P < 0.01) in the H1299 cells. Levels of oxidative stress markers were altered significantly ( P < 0.01) by matricin. Caspase-3, caspase-8, and caspase-9 levels were significantly increased ( P < 0.01) in matricin-treated H1299 cells. Western blot analysis showed decreased expression of anti-apoptotic Bcl-2, increased expressions of Bax and phosphorylated JNK, ERK 1/2, and p-38 MAPK proteins in matricin-treated H1299 cells. Matricin has significant anti-proliferative and apoptosis-inducing effects via activation of MAPK pathway in non-small cell lung cancer cells.

iScience ◽  
2021 ◽  
pp. 103224
Author(s):  
Rebecca Caeser ◽  
Christopher Hulton ◽  
Emily Costa ◽  
Vidushi Durani ◽  
Megan Little ◽  
...  

2021 ◽  
pp. 1-13
Author(s):  
Yonglu Li ◽  
Yaxuan Wang ◽  
Xin Yu ◽  
Ting Yu ◽  
Xiaodong Zheng ◽  
...  

2011 ◽  
Vol 113 (6) ◽  
pp. 1353-1364 ◽  
Author(s):  
Naomi Fujioka ◽  
Julia Nguyen ◽  
Chunsheng Chen ◽  
Yunfang Li ◽  
Teena Pasrija ◽  
...  

2018 ◽  
Vol 48 (4) ◽  
pp. 1433-1442 ◽  
Author(s):  
Jie Min ◽  
Hua Shen ◽  
Wang Xi ◽  
Qing Wang ◽  
Liang Yin ◽  
...  

Background/Aims: Caffeic acid (CA) is known to possess multiple biological activities including anti-cancer activities. However, the molecular mechanisms underlying these activities in non-small-cell lung cancer (NSCLC) cells are not fully understood. We attempted to clarify whether CA could enhance paclitaxel (PTX)-induced cytotoxicity in H1299 cells. Methods: First, we tested the cytotoxic effects in both H1299 cells and normal human Bease-2b cells by cell proliferation experiments. Next, we use Annexin V/propidium iodide apoptosis analysis and flow cytometric analysis to investigate apoptosis and cell cycle arrest under the treatments mentioned above. To further pinpoint changes in apoptosis, we tested the caspase-associated apoptotic pathway, which involves the activities of caspase-3 and caspase-9. Moreover, apoptosis-related proteins and MAPK pathway proteins were examined by western blot. An H1299 xenograft nude mice model was used to further evaluate the tumor-suppressing effects of CA and PTX in vivo. Results: Combination treatment with low-dose CA and PTX decreased the proliferation of NSCLC H1299 cells but not normal Beas-2b cells. Flow cytometry showed that H1299 cells were arrested in the sub-G1 phase and apoptosis was significantly increased in H1299 cells after CA treatment. Caspase-3 and caspase-9 activities were both increased after CA treatment. Furthermore, CA increased the PTX-induced activation of Bax, Bid, and downstream cleaved PARP, and phosphorylation of extracellular signal regulated kinase1/2 and c-Jun NH2-terminal protein kinase1/2. An in vivo tumor-suppression assay demonstrated that CA and PTX combined treatment exerted a more effective suppressive effect on tumor growth in H1299 xenografts without causing significant adverse effects. Conclusions: Our results indicated that CA inhibited NSCLC H1299 cell growth by inducing apoptosis and CA and PTX combined produced a synergistic anti-cancer effect in H1299 cells.


2019 ◽  
Vol 39 (5) ◽  
pp. 2437-2441 ◽  
Author(s):  
SINA ERCAN ◽  
SIBEL ARINC ◽  
SEDA GULEC YILMAZ ◽  
CIGDEM ALTUNOK ◽  
FERIDE YAMAN ◽  
...  

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