scholarly journals Target Identification of Oldenlandia diffusa Extract for Anticancer Property

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 329-329
Author(s):  
Da Gyeom Kang ◽  
Soo Jung Park ◽  
Yoon Jung Park
Keyword(s):  
Lung Cancer ◽  
Overall Survival ◽  
Ursolic Acid ◽  
A549 Cells ◽  
Indirect Evidence ◽  
Target Prediction ◽  
Dependent Manner ◽  
Expression Levels ◽  
Mutational Status ◽  
Oldenlandia Diffusa

Abstract Objectives Oldenlandia diffusa Rox has been known as a medicinal herb to treat lung and stomach cancer. However, its molecular mechanism has not been fully elucidated. This study was aimed to investigate the anticancer effects of Oldenlandia diffusa extract (EOD) and to identify a target of EOD. Methods EOD was extracted from dried Oldenlandia diffusa with 50% of ethanol, followed by quantification of ursolic acid (UA) and oleanolic acid (OA) as standard substances. To check the cytotoxiticity of EOD, MTT assay was performed for A2780 and A549 cells in various doses. Swiss Target prediction software was used to investigate the activity of UA and OA. cBioPortal and Oncomine Data were analyze for mutational status and RNA expression levels in diverse cancer cells of the candidate target, respectively. TCGA Data from Human Protein Atlas was used to query correlation between expression levels of candidate genes and overall survival times. Results EOD inhibited the growth of the cells in a dose-dependent manner. The 50% inhibitory concentration (IC50) for A2780 cell was 160 μg/mL of EOD for 48hrs and A549 cell viability was decreased to 75% at 800 μg/mL. Swiss Target prediction reports of two pentacyclic triterpene acids, UA and OA, revealed strong interactions with PTP1B in silico tests, which is indirect evidence of capacity. PTP1B mRNA expression was elevated in cancer cell, especially in lung and ovarian cancer. PTP1B amplification or over-expression was significantly associated with poor overall survival of ovarian and lung cancer patients. Conclusions These data suggests that PTP1B might be a direct target of EOD containing high level of ursolic acid to exert anti-cancer property in ovarian and lung cancer. Funding Sources This study was supported by the National Research Foundation of Korea to Y.J.P and S.J.P. DGK is grateful for financial support from Brain Korea Four Project (Education Research Center for 4IR-Based Health Care).

scholarly journals Hydrogen gas represses the progression of lung cancer via down-regulating CD47

2020 ◽  
Vol 40 (4) ◽  
Author(s):  
Jinghong Meng ◽  
Leyuan Liu ◽  
Dongchang Wang ◽  
Zhenfeng Yan ◽  
Gang Chen
Keyword(s):  
Lung Cancer ◽  
Molecular Mechanisms ◽  
A549 Cells ◽  
Hydrogen Gas ◽  
Cell Counting ◽  
Dependent Manner ◽  
Expression Levels ◽  
Invasion And Migration ◽  
Tumor Tissues ◽  
And Migration

Abstract Hydrogen gas (H2) has been identified to play an anti-tumor role in several kinds of cancers, but the molecular mechanisms remain largely unknown. In our previous study, our project group found that H2 could decrease the expression of CD47 in lung cancer A549 cells via the next-generation sequencing, indicating that CD47 might be involved in H2-mediated lung cancer repression. Therefore, the present study aimed to explore the effects of CD47 on H2-induced lung cancer repression. Western blotting and real-time PCR (RT-PCR) assays were used to detect the levels of proteins and mRNAs, respectively. Cell proliferation, invasion, migration and apoptosis were detected by using the cell counting kit-8 (CCK-8), Transwell chambers, wound healing and flow cytometry assays, respectively. The results showed that H2 treatment caused decreases in the expression levels of CD47 and cell division control protein 42 (CDC42) in a dose-dependent manner. Up-regulation of CD47 abolished H2 roles in promoting lung cancer cell apoptosis and repressing cell growth, invasion and migration in both A549 and H1975 cell lines. However, knockdown of CD47 enhanced H2 role in lung cancer inhibition. Moreover, we also observed that H2 treatment induced obvious inhibitions in the expression levels of CDC42 and CD47 in mice tumor tissues, as well as reinforced macrophage-mediated phagocytosis in A549 and H1975 cells. In conclusion, the current study reveals that H2 inhibits the progression of lung cancer via down-regulating CD47, which might be a potent method for lung cancer treatment.

scholarly journals Investigating Cytotoxic Effects and Molecular Mechanisms of Quinoa Seed Extract Against Human Lung Cancer Cell Lines

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Homa Mollaei ◽  
Farzaneh Karimi ◽  
Morteza Ghorbany ◽  
Mahboubeh Sadat Hosseinzadeh ◽  
Maryam Moudi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Viability ◽  
Cancer Cell ◽  
A549 Cells ◽  
Seed Extract ◽  
Human Lung Cancer ◽  
Dependent Manner ◽  
Lung Cancer Cell ◽  
Expression Levels ◽  
Seed Extracts

Background: Lung cancer is one of the most common leading causes of mortality and morbidity worldwide. Despite recent advances in therapeutic approaches, common methods are not fully effective. Thus, researchers are looking for some novel complementary agents to improve the effectiveness of therapies. Emerging evidence has shown the antitumor activity of several natural components such as quinoa seed extracts in various types of cancer. Objectives: Hence, this study was conducted to evaluate the antiproliferation and anti-apoptotic activity of quinoa on the A549 lung cancer cell line. Methods: The cell viability of A549 cells treated with quinoa was detected using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The expression levels of BAX and BCL2 as apoptosis-related genes were assessed using real-time polymerase chain reaction (PCR). Finally, the statistical analysis was performed using GraphPad Prism version 7. Results: Our findings demonstrated that the cell viability decreased in a concentration and time-dependent manner. Also, treating A549 cells with doses of 1.60 and 1.92 mg/mL of quinoa seed extracts could increase BAX and decrease BCL2 expression levels (P < 0.05). However, the higher dose (1.92 mg/mL) was significantly effective. Conclusions: According to this study, quinoa seed extract could induce apoptosis in lung cancer cells (A549) throughout the increased ratio of BAX/BCL2. However, further investigations are required to confirm the results.

scholarly journals Cytotoxic Effects of Flubendazole in Human Lung Cancer Cell Line A549

2020 ◽  
Vol 11 (4) ◽  
Author(s):  
Elham Hoveizi ◽  
Fatemeh Fakharzadeh Jahromi
Keyword(s):  
Lung Cancer ◽  
Cell Viability ◽  
Human Lung ◽  
A549 Cells ◽  
Beclin 1 ◽  
Human Lung Cancer ◽  
Pcr Analysis ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Acridine Orange Staining

Background: The development of effective anticancer drugs is a significant health issue. Previous studies showed that members of the benzimidazole family have anticancer effects on several cancers Objectives: The present study investigated the cytotoxic effect of flubendazole on A549 human lung cancer cells. Methods: The A549 cells were treated with flubendazole at 1, 2, 5, and 10 µM concentrations for three days. Cell viability was measured by the MTT assay and Acridine orange staining. Also, the expressions of P62 and Beclin -1 were analyzed by qRT-PCR analysis. Results: Cell viability of A549 cells, in a concentration-dependent manner, showed significant differences between the treatment and control groups, and the IC50 value was determined to be 2 µM. Also, flubendazole reduced the expression of P62 and increased the expression of Beclin 1 in treated cells. Conclusions: Flubendazole induces cell death in A549 cells in a dose and time-dependent manner and can offer new factors in lung cancer therapeutic strategies.

scholarly journals Osimertinib Improves Overall Survival in Patients with Leptomeningeal Metastases Associated with EGFR-Mutated Non-Small-Cell Lung Cancer Regardless of Cerebrospinal Fluid T790M Mutational Status

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Milan Zhang ◽  
Weifeng Ma ◽  
Huiqin Liu ◽  
Yushu Jiang ◽  
Lingzhi Qin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Overall Survival ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
T790m Mutation ◽  
Mutation Status ◽  
Mutational Status ◽  
Egfr Mutated

Osimertinib has demonstrated promising efficacy against leptomeningeal metastasis (LM) associated with T790M-positive non-small-cell lung cancer (NSCLC). However, the effect of cerebrospinal fluid’s (CSF’s) epidermal growth factor receptor (EGFR) T790M mutation on osimertinib efficacy remains unclear.Seventy-eight patients were studied with EGFR-mutated NSCLC and LM. Case data were collected and EGFR mutation status of circulating cell-free DNA from paired CSF, and plasma of 23 patients with LM was detected using droplet digital PCR. The median overall survival (mOS) was 8.08 months (95% CI: 6.07–10.09) in the study. Forty-four osimertinib-treated patients had an improved mOS of 13.15 (95% CI: 5.74–20.57) and a median progression-free survival (PFS) of 9.50 months (95% CI: 6.77–12.23) when compared with patients treated with first- or second-generation EGFR-TKI (mOS = 3.00 months (95% CI: 1.32–4.68) and median PFS = 1.50 months (95% CI: 0.00–3.14)). In the osimertinib group, mOS values for CSF with and without T790M mutation were 22.15 months (95% CI: 9.44–34.87) and 13.39 months (95% CI: 7.01–19.76), respectively, with no statistical differences. Regardless of the CSF T790M mutation status, osimertinib demonstrated significant efficacy against LM associated with NSCLC.

scholarly journals A dose- and time-dependent effect of oxythiamine on cell growth inhibition in non-small cell lung cancer

2021 ◽  
Author(s):  
Lin Bai ◽  
Hui-li Zhu
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Critical Role ◽  
A549 Cells ◽  
Small Cell ◽  
Time Dependent ◽  
Dependent Manner ◽  
Small Cell Lung

AbstractThe high mortality rate of non-small-cell lung cancer (NSCLC) is mostly due to the high risk of recurrence. A comprehensive understanding of proliferation mechanisms of NSCLC would remarkably contribute to blocking up the invasion and metastasis of tumor cells. In our previous study, the remarkable decreased activity of Thiamine-dependent enzymes (TDEs), involving in intermediary metabolism responsible for energy production of tumor, was found under conditions of thiamine deficiency in vivo. To explore the effect of Oxythiamine (OT), a TDEs antimetabolite, on cell growth, we co-cultured A549 cells with OT in vitro at various doses (0.1, 1, 10 and 100 μM) and time periods (6, 12, 24 and 48 h) and subsequent cell proliferation and apoptosis assays were performed respectively. Our findings demonstrated that A549 cells proliferation was significantly downregulated by OT treatment in a progressively dose as well as time dependent manner. Inhibition of TDEs resulted in antagonism of lung cancer growth by inducing cells to cease the cycle as well as apoptotic cell death. We concluded a critical role of OT, a TDEs antagonistic compound, indicating the potential target of its practical use.

Mechanism of interaction between TM4SF1 and jak2-stat3 signaling pathway in lung cancer cells and expression analysis in non-small cell lung cancer

2020 ◽  
Author(s):  
Yumeng Niu ◽  
Hailong Deng ◽  
Lipeng Li ◽  
Weikang Chen ◽  
Yuxuan Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Signaling Pathway ◽  
A549 Cells ◽  
Normal Lung ◽  
Expression Levels ◽  
Qrt Pcr ◽  
Stat3 Signaling ◽  
Skin Cancers ◽  
Stat3 Signaling Pathway ◽  
Cancer Tissues

Abstract Background According to the latest data released in 2018, it is estimated that there will be 18.1 million new cancer cases worldwide (excluding 1.7 million non-melanoma skin cancers) and 9.6 million cancer deaths (excluding 950 non-melanoma skin cancers) Million cases). Among them, the incidence of lung cancer (11.6% of the total number of cases) and mortality (18.4% of the total number of cancer deaths, which are expected to cause 1.8 million deaths) are the first. In recent years, studies have found TM4SF1 play an important role in the development process of many tumors.Methods Sixty-one patients with NSCLC who underwent surgical resection of cancer tissues, para-carcinoma tissues, and 10 normal lung tissues removed from benign lung disease (Jun/2018-Dec/2018) were collected. Real-time immunofluorescence quantitative PCR (qRT-PCR) and Western blot were used to detect the expression of TM4SF1 in NSCLC tissues (CT), para-carcinoma tissue (PCT), and normal lung tissues(NLT). TM4SF1 gene was overexpressed in lung cancer A549 cells using lentiviral transfection technology, qRT-PCR and Western blot were used to detect whether TM4SF1 gene was successfully expressed in lung cancer A549 cells, and Transwell was used to detect the effect of TM4SF1 overexpression on A549 migration. JAK2-STAT3 signal pathway interference reagent AG490 was used to analyze the expression levels of Stat3 and downstream Sox2 genes in the overexpression group, blank group, negative control group and their corresponding treatment groups TM4SF1, JAK2-STAT3 signal pathway using real-time qRT-PCR. Analyze the relevance of these three indicators at the same time.Results The expression levels of TM4SF1 mRNA and protein in cancer tissues were significantly higher than those in adjacent cancer tissues (P<0.05) and normal lung tissue specimens (P <0.05). The expression of TM4SF1 was not significantly associated with the age and sex of patients, but was associated with tumor size, degree of differentiation, lymph node metastasis, and clinical stage were related (P<0.05). TM4SF1 was successfully overexpressed in A549 cells. After overexpressing TM4SF1, the ability to migrate of A549 cells was significantly enhanced, and the expression levels of Stat3 and downstream Sox2 in the JAK2-STAT3 signaling pathway were up-regulated. The expression of TM4SF1, Stat3 and Sox2 at the mRNA level showed a positive correlation trend (P<0.01).Conclusion TM4SF1 is highly expressed in NSCLC, and its expression level is closely related to many clinical staging indicators. Overexpression of this gene can promote the migration of A549 cells and up-regulate the expression levels of Stat3 and downstream Sox2 in the JAK2-STAT3 signaling pathway. The expressions of TM4SF1, Stat3 and Sox2 were positively correlated in A549 cells. TM4SF1 may promote the occurrence, development and distant metastasis of NSCLC through this pathway. TM4SF1 may become a potential therapeutic target for NSCLC.

scholarly journals EVALUATION OF IN VITRO CYTOTOXIC EFFECT OF VIOLACEIN PRODUCED BY NOVEL ISOLATE CHROMOBACTERIUM VACCINII CV5 AGAINST THE CERVICAL AND LUNG CANCER CELL

2017 ◽  
Vol 10 (10) ◽  
pp. 227 ◽  
Author(s):  
Vishnu T Santhosh ◽  
Palaniswamy Muthusamy
Keyword(s):  
Lung Cancer ◽  
Anticancer Activity ◽  
Cell Lines ◽  
Cancer Cell ◽  
A549 Cells ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Cytotoxicity Activity ◽  
Ic50 Values

  Objectives: This study investigates the in vitro anticancer activity of the violacein extracted from the Chromobacterium vaccinii CV5.Methods: Natural colorants or dyes derived from flora to fauna are believed to be safe because of nontoxic, noncarcinogenic, and biodegradable in nature. There are a number of natural pigments, but only a few are available in sufficient quantities for industrial production. The cytotoxicity activity of pigment was assessed against the cervical (HeLa) and lung cancer (A549) cell lines using the MTT assay and there by potential cytotoxic activity exhibited by the pigment was identified.Results: The result of the pigment shows potent anticancer activity on the two cancer cell lines tested in a concentration dependent manner. The potent anticancer activity was observed with the pigment with IC50 values of 26 μg/mL on HeLa and 31 μg/mL on A549 cells, respectively.Conclusion: The study is pioneering report for determining the better in vitro anticancer activity of violacein from the novel isolate C. vaccinii CV5.

scholarly journals (E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one (BCI) induces apoptosis via the intrinsic pathway in H1299 lung cancer cells

2017 ◽  
Author(s):  
Jong-Woon Shin ◽  
Sae-Bom Kwon ◽  
Yesol Bak ◽  
Sangku Lee ◽  
Do-Young Yoon
Keyword(s):  
Lung Cancer ◽  
Cell Viability ◽  
Morphological Changes ◽  
A549 Cells ◽  
Fluorescein Isothiocyanate ◽  
Receptor Expression ◽  
Dependent Manner ◽  
Intrinsic Pathway ◽  
Extrinsic Pathway ◽  
Dose Dependent

Abstract(E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one (BCI) is known as a dual specific phosphatase 1/6 or MAPK inhibitor. However, its precise anti-lung cancer mechanism remains unknown. In this study, the effects of BCI on cell viability were investigated in the non-small cell lung cancer cell lines NCI-H1299, A549, and NCI-H460. We confirmed that BCI significantly inhibited the cell viability of NCI-H1299 compared to those of NCI-H460 and A549 cells. The anti-cancer effects of BCI were evaluated by MTS assay, annexin V-fluorescein isothiocyanate/propidium iodide staining, cell cycle analysis, reverse transcription-PCR, western blotting, and JC-1 staining in NCI-H1299 cells. BCI induced cellular morphological changes and inhibited viability of NCI-H1299 cells in a dose-dependent manner. BCI enhanced Bax expression and induced processing of caspase-9, caspase-3, and poly (ADP-ribose) polymerase as well as the release of cytochrome c from the mitochondria into the cytosol. BCI also down-regulated Bcl-2 expression but enhanced Bax expression in a dose-dependent manner in NCI-H1299 cells. In addition, BCI did not modulate death receptor expression or the extrinsic factor caspase-8 and Bid, a linker between the intrinsic and extrinsic apoptotic pathways in NCI-H1299 cells. On the basis of these results, we conclude that BCI induces apoptosis through a mediated intrinsic pathway, but not extrinsic pathway in NCI-H1299 cells. These results suggest that BCI can be used as a therapeutic agent in lung cancer.

scholarly journals Up-Regulation of p53/miR-628-3p Pathway, a Novel Mechanism of Shikonin on Inhibiting Proliferation and Inducing Apoptosis of A549 and PC-9 Non–Small Cell Lung Cancer Cell Lines

2021 ◽  
Vol 12 ◽  
Author(s):  
Jieli Pan ◽  
Meiya Li ◽  
Fenglin Yu ◽  
Feiye Zhu ◽  
Linyan Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Treatment Strategies ◽  
A549 Cells ◽  
Direct Interaction ◽  
Promoter Sequence ◽  
Small Cell ◽  
Dependent Manner ◽  
Small Cell Lung

Shikonin (SHK) is a pleiotropic agent with remarkable cell growth inhibition activity against various cancer types, especially non–small cell lung cancer (NSCLC), but its molecular mechanism is still unclear. Our previous study found that miR-628-3p could inhibit the growth of A549 cells and induce its apoptosis. Bioinformatics analysis predicted that miR-628-3p promoter sequence contained p53 binding sites. Considering the regulatory effect of SHK on p53, we speculate that SHK may inhibit the growth and induce apoptosis of NSCLC cells by up-regulating miR-628-3p. CCK-8 and EdU assay confirmed the inhibitory effect of SHK on A549 and PC-9 cells. Meanwhile, quantitative reverse transcription–polymerase chain reaction and Western blot showed that SHK could promote the expression of p53 and miR-628-3p in a dose-dependent manner. Overexpression of p53 or miR-628-3p can inhibit the growth and promote apoptosis of A549 and PC-9 cells, while silencing p53 or miR-628-3p has the opposite effect. Dual luciferase reporting assay and ChIP (chromatin immunoprecipitation) assay further verified the direct interaction between p53 and the promoter of miR-628-3p. Gene knockdown for p53 or miR-628-3p confirmed that SHK inhibits the growth and induces apoptosis of A549 and PC-9 cells at least partly by up-regulating p53/miR-628-3p signaling pathway. Therefore, these novel findings provide an alternative approach to target p53/miR-628-3p axis and could be used for the development of new treatment strategies for NSCLC.

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