|Year : 2019 | Volume
| Issue : 2 | Page : 247-248
The role of platelets in the process of lung cancer A549 cell growth and its related mechanism
Li Juan, Zhangfei Wang, Man Fang, Yiqin Luo
Department of Blood Transfusion, The First Affiliated Hospital of University of Science and Technology of China, Hefei, Anhui Province, China
|Date of Submission||28-Sep-2019|
|Date of Acceptance||28-Sep-2019|
|Date of Web Publication||17-Oct-2019|
Dr. Yiqin Luo
Department of Blood Transfusion, The First Affiliated Hospital of University of Science and Technology of China, Hefei, Anhui Provinc
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Juan L, Wang Z, Fang M, Luo Y. The role of platelets in the process of lung cancer A549 cell growth and its related mechanism. Glob J Transfus Med 2019;4:247-8
|How to cite this URL:|
Juan L, Wang Z, Fang M, Luo Y. The role of platelets in the process of lung cancer A549 cell growth and its related mechanism. Glob J Transfus Med [serial online] 2019 [cited 2021 Oct 24];4:247-8. Available from: https://www.gjtmonline.com/text.asp?2019/4/2/247/269403
This special communication reproduced with permission from Journal of Clinical Transfusion and Lab Medicine
| Introduction|| |
Lung cancer is one of the most common malignant tumors; both its morbidity and mortality rate is on the rise. At present, the mortality rate of lung cancer has been the first. Infinite proliferation and metastasis are the major reasons of death in lung cancer, which also provides a conundrum for clinical treatment. As early as 1865, Trousseau had found the correlation between platelets (PLTs) and tumor. Malignant tumor is high coagulation state and common and rich in microthrombus of PLTs. A growing number of studies reported also confirmed that PLTs promoted the development of tumor. Therefore, this research explored the biological effects of PLT on lung adenocarcinomain vitro and studied the role of PLTs in chemotherapy-induced cancer cell death and survival, which could offer a new breakthrough point for early prevention and treatment of tumor.
| Methods|| |
Flow cytometry was performed to detect the apoptotic effect on A549 by PLT and the effect of PLT on chemotherapy drug. Lung adenocarcinoma A549 cell line was stimulated with PLT (4.0 × 107/ml) at different time (0 h, 12 h, 24 h, and 48 h); then, Western blotting was used to detect the protein expression of extracellular signal regulated kinase (ERK) 1/2, c-Jun N-terminal kinase (JNK), p-ERK, p-JNK, matrix metalloproteinase (MMP) 2, MMP-9, the Bcl-2, and Bax level in the cells treated with or without (as control) PLTs.
| Results|| |
The apoptotic effect on A549 by PLTs and the effect of PLT on chemotherapy drug were detected by flow cytometry see [Figure 1]. Western blot showed that ERK1/2, JNK, p-ERK, p-JNK, MMP-2, MMP-9, and Bcl-2 expression were significantly increased, and the expression of Bax was decreased obviously, compared to control group see [Figure 2].
|Figure 1: Platelets decrease drug-induced cancer cell apoptosis of A549 cells in the presence of gemcitabine. (a) Representative (three experiments) dot plots of A549 cells following 24 h of incubation in the presence of serum-free medium. (b) Representative (three experiments) dot plots of A549 cells following 24 h of incubation in the presence of platelets (PLT, 4.0 × 107/ml). (c) Representative (three experiments) dot plots of gemcitabine-treated (gemcitabine, 200 ug/ml) A549 cells following 24 h of incubation in the presence of platelets (PLT, 4.0 × 107/ml). (d) Representative (three experiments) dot plots of A549 cells following 24 h of incubation in the presence of gemcitabine (gemcitabine, 200 ug/ml). (e) The comparison among the histograms of the four experiments. Q1: Necrosis, Q2: Late apoptosis, Q3: Live cells, and Q4: Early apoptosis|
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|Figure 2: Western blot analysis of (a) extracellular signal-regulated kinase, c-Jun N-terminal kinase, p-extracellular signal-regulated kinase, p- c-Jun N-terminal kinase, (b) Bcl-2, BAX, (c) matrix metalloproteinase-2, matrix metalloproteinases-9 in A549 cell treated with 4.0 × 107/ml platelets for different times|
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| Discussion and Conclusion|| |
PLTs stimulated growth and migration of A549 cells in vitro, which were positively correlated with PLT concentration. PLTs stimulated the expression of ERK1/2, JNK, p-ERK, p-JNK, MMP-2, and MMP-9 in MAPKs to promote proliferation and metastasis of lung adenocarcinoma.
The resistance of tumor chemotherapy drug by PLTs showed that PLTs may be potential treatment targets for lung adenocarcinoma in combination with chemotherapy drug. Limitation of current study is that we are yet to solve the problem in the perspective of genetics and if PLTs play the same role from other signaling pathways. Although it has been found that MMP-2 and MMP-9 are increased when tumor cells are allowed to interact with PLTs and MMPs are regulated at gene level by different mediators, including MAPK family, the signal pathways leading to MMPs production remain poorly understood.
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Conflicts of interest
There are no conflicts of interest.
[Figure 1], [Figure 2]