The Effect of Terpenoid Natural Chinese Medicine Molecular Compound on Lung Cancer Treatment

Among all malignant tumors in the whole universe, the incidence and mortality of lung cancer disease rank first. Especially in the past few years, the occurrence of lung cancer in the urban population has continued to increase, which seriously threatens the lives and health of people. Among the many treatments for lung cancer, chemotherapy is the best one, but traditional chemotherapy has low specificity and drug resistance. To address the above issue, this study reviews the five biological pathways that common terpenoid compounds in medicinal plants interfere with the occurrence and development of lung cancer: cell proliferation, cell apoptosis, cell autophagy, cell invasion, metastasis, and immune mechanism regulation. In addition, the mechanism of the terpenoid natural traditional Chinese medicine monomer compound combined with Western medicine in the multipathway antilung cancer is summarized.

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Inhibition of lung cancer cell proliferation mediated by human mesenchymal stem cells

Acta Biochimica et Biophysica Sinica ◽

10.1093/abbs/gmq118 ◽

2010 ◽

Vol 43 (2) ◽

pp. 143-148 ◽

Cited By ~ 29

Author(s):

L. Li ◽

H. Tian ◽

Z. Chen ◽

W. Yue ◽

S. Li ◽

...

Keyword(s):

Lung Cancer ◽

Stem Cells ◽

Cell Proliferation ◽

Mesenchymal Stem Cells ◽

Cancer Cell ◽

Human Mesenchymal Stem Cells ◽

Cancer Cell Proliferation ◽

Lung Cancer Cell

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Polyamide Amine Dendrimer Nanoparticles Conjugated with Cis-Diamminedichloroplatinum (CDDP) and miRNA-200c Inhibitor Suppresses Lung Cancer Cell Proliferation

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2021.2822 ◽

2021 ◽

Vol 11 (9) ◽

pp. 1760-1768

Author(s):

Fang Zhang ◽

Jili Zou ◽

Dandan Huang

Keyword(s):

Lung Cancer ◽

Cell Proliferation ◽

Cancer Cell Proliferation ◽

Lung Cancer Cell ◽

Targeting Delivery ◽

Apoptosis Related Protein ◽

Related Proteins ◽

Exclusion Method ◽

Inhibit Cell Proliferation ◽

Excellent Stability

Our study elucidates the effect of folate polyamide amine dendrimer nanoparticles targeting delivery of miRNA-200c inhibitor and CDDP on lung cancer cells proliferation. We established polyamide amine dendrimer nanoparticles binding with CDDP and miRNA-200c inhibitor (Den-PEI-CDDP-siRNA-FA), TEM was employed to detect the morphology of nanoparticles. Agarose gel assay was selected for stabilization test. Cell proliferation were detected by trypanosoma blue exclusion method. The expression of miRNA-200c targeted APKPA12 and apoptosis-related proteins were detected by Western blot and PCR. Finally, apoptosis was analyzed by flow cytometry. Den-PEI-CDDP-siRNA-FA nanoparticles showed excellent stability and drug encapsulation ability. Nanoparticles targeting for FRA to co-deliver siRNA and CDDP could significantly promote cell apoptosis, increase apoptosis-related protein expression, and inhibit cell proliferation. Besides, nanoparticles exerted less venomous effect than untargeted nanoparticles in MRC9 lung fibroblast. Den nanoparticle targeting FRA might be used as the carrier for joint applications with siRNA and CDDP for treating lung cancer.

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Long non-coding RNA FGD5-AS1 promotes non-small cell lung cancer cell proliferation through sponging hsa-miR-107 to up-regulate FGFRL1

Bioscience Reports ◽

10.1042/bsr20193309 ◽

2020 ◽

Vol 40 (1) ◽

Cited By ~ 5

Author(s):

Yafeng Fan ◽

Hongxia Li ◽

Zhongping Yu ◽

Wen Dong ◽

Xiaoyan Cui ◽

...

Keyword(s):

Lung Cancer ◽

Cell Proliferation ◽

Small Cell Lung Cancer ◽

Cancer Cell ◽

Small Cell ◽

Cancer Cell Proliferation ◽

Lung Cancer Cell ◽

Small Cell Lung ◽

Non Coding Rna ◽

Long Non Coding Rna

Abstract Long non-coding RNA (lncRNA) FYVE, RhoGEF and PH domain containing 5 antisense RNA 1 (FGD5-AS1) has been reported as an oncogene in colorectal cancer, promoting its tumorgenesis. The present paper focused on searching the potential function of FGD5-AS1 in non-small cell lung carcinoma (NSCLC). There are connections between the expression of lncRNA FGD5-AS1 and human NSCLC tumor growth and progression. Also, the relationships between FGD5-AS1, hsa-miR-107 and mRNA fibroblast growth factor receptor like 1 (FGFRL1) are going to test their interaction in NSCLC cell lines, which may cause a series of biological behaviors of NSCLC cells. qRT-PCR analysis was conducted to test the expression of RNAs in different situation. CCK-8 experiment and clone formation assay were performed to assess proliferation of NSCLC cells. Also, connection between FGD5-AS1 and hsa-miR-107 were investigated by luciferase reporter assay and RNA pull-down assay. Rescue experiments were performed to verify the modulating relationship between FGD5-AS1, hsa-miR-107 and FGFRL1. High-level expression of FGD5-AS1 was found in NSCLC. FGD5-AS1 may promote the proliferation of NSCLC cells. Also, the combination between hsa-miR-107, FGD5-AS1 and NSCLC have been proved, which means they can play an interaction function in NSCLC cells. Thence, we concluded that lncRNA FGD5-AS1 promotes non-small cell lung cancer cell proliferation through sponging hsa-miR-107 to up-regulate FGFRL1.

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A survey of primary lung cancer among NTT workers in the Tokyo area. The incidence and mortality during the past 30 years and significance of radiologic screening

Lung Cancer ◽

10.1016/0169-5002(94)90304-2 ◽

1994 ◽

Vol 11 (1-2) ◽

pp. 126

Keyword(s):

Lung Cancer ◽

Primary Lung Cancer ◽

The Past ◽

Incidence And Mortality

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A Review of the Histopathology of Cigarette Smoke–Induced Lung Cancer in Rats and Mice

International Journal of Toxicology ◽

10.1080/10915810701483450 ◽

2007 ◽

Vol 26 (4) ◽

pp. 307-313 ◽

Cited By ~ 16

Author(s):

Fletcher F. Hahn ◽

Andrew P. Gigliotti ◽

Julie A. Hutt ◽

Thomas H. March ◽

Joe L. Mauderly

Keyword(s):

Lung Cancer ◽

Cigarette Smoke ◽

Malignant Tumors ◽

Lung Tumors ◽

The Past ◽

Lifetime Exposure ◽

Low Incidence ◽

Epithelial Lesions ◽

Induced Changes ◽

Rats And Mice

In the past several years an increased number of lung tumors has been reported in laboratory studies of rats and mice after lifetime exposure to mainstream cigarette smoke. Proliferative epithelial lesions are present in the lungs of both species and are apparent antecedent lesions to benign and malignant tumors. Both species have alveolar epithelia hyperplasia, alveolar adenomas, and alveolar carcinomas. The incidence of all three are more in the rats. In addition, mice also have bronchiolar epithelial hyperplasia and bronchial papillomas not found in rats. Rats have a low incidence of squamous cyst that is not found in mice. Lung tumors in rats and mice are found at the end of the life span and rarely metastasize. The characteristics of the lung tumors, and the proliferative changes associated with the tumors, are important in helping understand the mechanisms of lung cancer induction. These studies in rats and mice allow new approaches to the study of cigarette smoke–induced changes in the lung.

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