scholarly journals Mahonia aquifolium Extracts Promote Doxorubicin Effects against Lung Adenocarcinoma Cells In Vitro

Molecules ◽  
2020 ◽  
Vol 25 (22) ◽  
pp. 5233 ◽  
Author(s):  
Ana Damjanović ◽  
Branka Kolundžija ◽  
Ivana Z. Matić ◽  
Ana Krivokuća ◽  
Gordana Zdunić ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Lung Adenocarcinoma ◽  
Colony Formation ◽  
Phase Distribution ◽  
Synergistic Effects ◽  
Cycle Phase ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells ◽  
Mahonia Aquifolium

Mahonia aquifolium and its secondary metabolites have been shown to have anticancer potential. We performed MTT, scratch, and colony formation assays; analyzed cell cycle phase distribution and doxorubicin uptake and retention with flow cytometry; and detected alterations in the expression of genes involved in the formation of cell–cell interactions and migration using quantitative real-time PCR following treatment of lung adenocarcinoma cells with doxorubicin, M. aquifolium extracts, or their combination. MTT assay results suggested strong synergistic effects of the combined treatments, and their application led to an increase in cell numbers in the subG1 phase of the cell cycle. Both extracts were shown to prolong doxorubicin retention time in cancer cells, while the application of doxorubicin/extract combination led to a decrease in MMP9 expression. Furthermore, cells treated with doxorubicin/extract combinations were shown to have lower migratory and colony formation potentials than untreated cells or cells treated with doxorubicin alone. The obtained results suggest that nontoxic M. aquifolium extracts can enhance the activity of doxorubicin, thus potentially allowing the application of lower doxorubicin doses in vivo, which may decrease its toxic effects in normal tissues.

scholarly journals Effect of shRNA-Mediated Knockdown EBF1 Gene Expression on the Proliferation of Lung Cancer Cell Line A549 In Vitro and In Vivo

2021 ◽  
Author(s):  
Lin WANG ◽  
Ding Li ◽  
Li REN ◽  
Honglei FENG
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Cell Cycle ◽  
Lung Adenocarcinoma ◽  
A549 Cells ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells ◽  
Cancer Tissues ◽  
Experimental Group

Abstract BackgroundThe incidence of lung cancer is increasing year by year. The study on the proliferation and metastasis of lung adenocarcinoma cells is of positive significance to improve the prognosis of patients with lung adenocarcinoma, but there is still a lack of more effective treatment for the proliferation and metastasis of lung adenocarcinoma cells .Here we find that a lymphocyte lineage specific transcription factor,EBF1, is frequently expressed in human lung cancer tissues and affects the proliferation of tumor cells , Objective to explore the possible mechanism of affecting the proliferation of lung adenocarcinoma cells.MethodsImmunohistochemistry and PCR were used to detect the expression of EBF1 in lung cancer tissues and lung cancer cell lines. According to the interference RNA (shRNA) sequence designed by our laboratory for EBF1 as the target sequence and a random sequence as the negative control, the recombinant retrovirus was constructed and transfected into A549 cells, which were used as A549-shRNA-EBF1 and A549-shRNA-control of experimental group and control group respectively; Knockdown of EBF1 gene was detected by PCR and Western blot. MTT and BrdU staining were used to detect the effect of EBF1-shRNA on the proliferation of A549 cells in vitro;flow cytometry was used to analyze the cell cycle of each group; subcutaneous inoculation of cells in axilla of nude mice was used to observe the effect of EBF1-shRNA on the tumorigenicity of A549 cells in nude mice; Western blot was used to detect the expression of CDK6, P21 and P27 proteins.ResultsEBF1 was not expressed in stromal cells of adjacent tissues and lung cancer tissues, but in nuclei of NSCLC and SCLC cancer cells. EBF1-shRNA knockdown EBF1 gene expression effectively; knockdown EBF1 gene expression can inhibit the proliferation of A549 cells in vitro and in vivo, and block the cell cycle of experimental group at G1 phase; after knockdown EBF1 gene expression, CDK6 protein expression in experimental group cells decreases, while P21 and P27 protein increase.ConclusionsEBF1-shRNA can inhibit the proliferation of lung adenocarcinoma A549 in vitro and in vivo by blocking cell cycle in G1 phase, which involves the decrease of CDK6 expression and the up-regulation of P21 and P27 expression. This study will supplement the theory that heterotopic expression of hematogenous transcription factors in lung cancer affects tumor proliferation and discover new molecular targets for cancer therapy.

scholarly journals PD-L1 lncRNA splice promotes lung adenocarcinoma progression via enhancing c-Myc activity

2020 ◽  
Author(s):  
Shuang Qu ◽  
Zichen Jiao ◽  
Geng Lu ◽  
Bing Yao ◽  
Ting Wang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Great Promise ◽  
Non Coding Rna ◽  
Adenocarcinoma Cells ◽  
T Cell Immune Responses ◽  
Lung Adenocarcinoma Cells ◽  
Novel Strategy ◽  
L1 Protein

ABSTRACTAlthough blockade of programmed death-ligand 1 (PD-L1) to enhance T cell immune responses shows great promise in tumor immunotherapy, the efficacy of such immune-checkpoint inhibition strategy is limited for patients with solid tumors. The mechanism underlying the limited efficacy of PD-L1 inhibitors remains unclear. Here, we show that human lung adenocarcinoma, regardless of PD-L1 protein positive or negative, all produce a long non-coding RNA isoform of PD-L1 (PD-L1-lnc) via alternative splicing, which promotes lung adenocarcinoma proliferation and metastasis. PD-L1-lnc in various lung adenocarcinoma cells is significantly upregulated by IFNγ in a manner similar to PD-L1 mRNA. Both in vitro and in vivo studies demonstrate that PD-L1-lnc increases proliferation and invasion but decreases apoptosis of lung adenocarcinoma cells. Mechanistically, PD-L1-lnc directly binds to c-Myc and enhances c-Myc transcriptional activity downstream in lung adenocarcinoma cells. Our results provide targeting PD-L1-lnc−c-Myc axis as a novel strategy for lung cancer therapy.

Ginsenoside Rk1 induces apoptosis and downregulates the expression of PD-L1 by targeting the NF-κB pathway in lung adenocarcinoma

2020 ◽  
Vol 11 (1) ◽  
pp. 456-471 ◽  
Author(s):  
Manling Hu ◽  
Jing Yang ◽  
Linlin Qu ◽  
Xuqian Deng ◽  
Zhiguang Duan ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Lung Adenocarcinoma ◽  
Cell Cycle Arrest ◽  
Cycle Arrest ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells

Ginsenoside Rk1 can function as an antitumor modulator that induces apoptosis in lung adenocarcinoma cells by inhibiting NF-κB transcription and triggering cell cycle arrest.

scholarly journals Kinesin Family Member 18A (KIF18A) Contributes to the Proliferation, Migration, and Invasion of Lung Adenocarcinoma Cells In Vitro and In Vivo

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Fu-Tao Chen ◽  
Fu-Kuan Zhong
Keyword(s):  
Tumor Growth ◽  
Lung Adenocarcinoma ◽  
Clinical Stage ◽  
Migration And Invasion ◽  
Expression Levels ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells ◽  
Tumor Growth And Metastasis

Objective. To determine the expression levels of KIF18A in lung adenocarcinoma and its relationship with the clinicopathologic features of patients undergoing radical colectomy and explore the potential role in the progression of lung adenocarcinoma. Methods. Immunohistochemical assays were performed to explore the expression levels of KIF18A in 82 samples of lung adenocarcinoma and corresponding normal tissues. According to the levels of KIF18A expression in lung adenocarcinoma tissue samples, patients were classified into the KIF18A high expression group and low expression group. Clinical data related to the perioperative clinical features (age, gender, smoking, tumor size, differentiation, clinical stage, and lymph node metastasis), the potential correlation between KIF18A expression levels, and clinical features were analyzed, and the effects of KIF18A on lung adenocarcinoma cell proliferation, migration, and invasion were measured by colony formation assay, MTT assay, wound healing assay, and transwell assays. The possible effects of KIF18A on tumor growth and metastasis were measured in mice through tumor growth and tumor metastasis assays in vivo. Results. KIF18A in lung adenocarcinoma tissues. Further, KIF18A was significantly associated to clinical characteristic features including the tumor size (P=0.033) and clinical stage (P=0.041) of patients with lung adenocarcinoma. Our data also investigated that KIF18A depletion dramatically impairs the proliferation, migration, and invasion capacity of lung adenocarcinoma cells in vitro and inhibits tumor growth and metastasis in mice. Conclusions. Our study reveals the involvement of KIF18A in the progression and metastasis of lung adenocarcinoma and provides a novel therapeutic target for the treatment of lung adenocarcinoma.

The effects of the electro-photodynamic in vitro treatment on human lung adenocarcinoma cells

2010 ◽  
Vol 79 (1) ◽  
pp. 90-94 ◽  
Author(s):  
Jolanta Saczko ◽  
Mariola Nowak ◽  
Nina Skolucka ◽  
Julita Kulbacka ◽  
Malgorzata Kotulska
Keyword(s):  
Lung Adenocarcinoma ◽  
Human Lung ◽  
Human Lung Adenocarcinoma ◽  
Adenocarcinoma Cells ◽  
Human Lung Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells ◽  
In Vitro Treatment
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