microRNA-1236-3p regulates DDP resistance in lung cancer cells

AbstractLung cancer is a malignant tumor leading to the most cancer-related deaths worldwide. The treatment efficiency of lung cancer remains poor mainly due to chemotherapy drug resistance, including cisplatin. MicroRNAs (miRNAs) are closely related to chemotherapy resistance of tumor cells. Here, we illustrated the underlying mechanism of miR-1236-3p on the DDP resistance in lung cancer cells. In this study, we found that the expression level of miR-1236-3p was significantly decreased in lung cancer tissues and A549 cell line. In addition, the half maximal inhibitory concentration (IC50) of DDP in A549 cells was significantly lower than that in A549/DDP cells, while the expression level of miR-1236-3p was prominently down-regulated in A549/DDP cells. Combining the online tool TargetScan and a dual-luciferase reporter assay, tumor protein, translationally-controlled 1 (TPT1) was proved to be the direct target gene of miR-1236-3p. The MTT and flow cytometry assays demonstrated that up-regulation of miR-1236-3p could markedly inhibit A549/DDP cell proliferation but promote apoptosis, which could be significantly reversed by pcDNA3.1-TPT1 plasmids. Finally, we further demonstrated that miR-1235-3p could restrain the expression levels of TPT1, Pim-3, phosphate-Bcl-2-associated death promoter (p-BAD) and B-cell lymphoma-extra large (Bcl-XL) in A549/DDP cells, while the inhibition could be reversed by pcDNA3.1-TPT1 as well. In a word, our study demonstrated that miR-1236-3p could reverse DDP resistance by modulation of TPT1 gene and inhibition of Pim-3 signaling pathway in lung cancer cells.

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miR-342-3p Regulates the Proliferation and Apoptosis of NSCLC Cells by Targeting BCL-2

Technology in Cancer Research & Treatment ◽

10.1177/15330338211041193 ◽

2021 ◽

Vol 20 ◽

pp. 153303382110411

Author(s):

Zhongjie Chen ◽

Junjie Ying ◽

Wenjun Shang ◽

Dongxiao Ding ◽

Min Guo ◽

...

Keyword(s):

Lung Cancer ◽

B Cell ◽

Cancer Cells ◽

Cell Lung Cancer ◽

Cell Lymphoma ◽

B Cell Lymphoma ◽

Nonsmall Cell Lung Cancer ◽

Lung Cancer Cells ◽

Luciferase Reporter ◽

Underlying Mechanisms

microRNA-342-3p plays an important role in tumor occurrence and development. However, the expression pattern and roles of microRNA-342-3p in nonsmall cell lung cancer remain poorly understood. In the current study, we explored the roles and underlying mechanisms of microRNA-342-3p in nonsmall cell lung cancer via gain- and loss-of-function analyses. We used quantitative reverse-transcription-polymerase chain reaction and western blotting assays to measure the expression levels of microRNA-342-3p in nonsmall-cell lung cancer and B-cell lymphoma-2. Furthermore, we used small interfering RNA and RNA mimics to analyze the functions and underlying mechanisms of microRNA-342-3p in nonsmall cell lung cancer cells. A luciferase reporter assay was performed to evaluate the direct binding site of the 5′-untranslated region of B-cell lymphoma-2 targeted by microRNA-342-3p. We found that the expression of microRNA-342-3p was significantly lower in nonsmall cell lung cancer cells and tissues than in normal cells and tissues. The upregulation of microRNA-342-3p suppressed cell proliferation while promoting apoptosis in H1975, H460, and H226 cells. The overexpression of microRNA-342-3p in nonsmall cell lung cancer cells led to the downregulation of mRNA and protein levels in B-cell lymphoma-2 cells. Thus, B-cell lymphoma-2 was identified as a direct target of microRNA-342-3p. These findings indicate that microRNA-342-3p inhibits the growth of nonsmall cell lung cancer by repressing the expression of B-cell lymphoma-2, which suggests that microRNA-342-3p could be a potential target for the treatment of nonsmall cell lung cancer.

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Sevoflurane induces lung cancer cell apoptosis via inhibition of the expression of miRNA155 gene

Tropical Journal of Pharmaceutical Research ◽

10.4314/tjpr.v20i1.11 ◽

2021 ◽

Vol 20 (1) ◽

pp. 69-74

Author(s):

Huaizhao Wang ◽

Bin Wang ◽

Jingyan Jing ◽

Na Li

Keyword(s):

Lung Cancer ◽

Lung Adenocarcinoma ◽

Cancer Cells ◽

Cell Apoptosis ◽

A549 Cells ◽

Underlying Mechanism ◽

Lung Cancer Cells ◽

Control Group ◽

Sevoflurane Group ◽

Lung Adenocarcinoma A549

Purpose: To determine the apoptotic effect of sevoflurane on lung cancer cells, and the underlying mechanism of action.Methods: Lung adenocarcinoma A549 cells were cultured for 24 h and divided into control group, 1% sevoflurane group and 3% sevoflurane group. The two levels of sevoflurane were provided through a gas monitor connected to each of the sevoflurane groups. The control group was not treated. Flow cytometry was used to analyze A549 cell apoptosis, while qRT-PCR was used for assay of the levels of miRNA155 in A549 cells. The protein expression of Bcl-2 was determined with immunoblotting. The percentage of apoptosis and levels of miRNA155 and Bcl-2 in the two cell lines were compared.Results: Significant differences in miRNA146a level were seen between the 3 % sevoflurane and control groups at 3 h. There was higher apoptosis in the 3 % sevoflurane group, relative to control, but miRNA155 levels in the 3 % sevoflurane group were generally less than that of the control (p < 0.05). There was lower Bcl-2 content in the 3 % sevoflurane group than in control group (p < 0.05).Conclusion: Sevoflurane exerts strong apoptotic and anti-proliferative effects on lung adenocarcinoma A549 cells via a mechanism which may be related to the downregulation of miRNA155, thereby inhibiting the expression of anti-apoptotic protein Bcl-2. This provides a new direction for research on anti-lung adenocarcinoma drugs. Keywords: Sevoflurane, Lung cancer cells, Apoptosis, Inhibition, miRNA155, Expression, Induction

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Improved Therapeutic Efficacy of Topotecan Against A549 Lung Cancer Cells with Folate-targeted Topotecan Liposomes

Current Drug Metabolism ◽

10.2174/1389200221999200820163337 ◽

2020 ◽

Vol 21 (11) ◽

pp. 902-909

Author(s):

Jingxin Zhang ◽

Weiyue Shi ◽

Gangqiang Xue ◽

Qiang Ma ◽

Haixin Cui ◽

...

Keyword(s):

Lung Cancer ◽

Drug Delivery ◽

Cancer Cells ◽

Targeted Delivery ◽

Therapeutic Efficacy ◽

Drug Delivery Systems ◽

Lung Tumor ◽

A549 Cells ◽

Delivery Systems ◽

Lung Cancer Cells

Background: Among all cancers, lung cancer has high mortality among patients in most of the countries in the world. Targeted delivery of anticancer drugs can significantly reduce the side effects and dramatically improve the effects of the treatment. Folate, a suitable ligand, can be modified to the surface of tumor-selective drug delivery systems because it can selectively bind to the folate receptor, which is highly expressed on the surface of lung tumor cells. Objective: This study aimed to construct a kind of folate-targeted topotecan liposomes for investigating their efficacy and mechanism of action in the treatment of lung cancer in preclinical models. Methods: We conjugated topotecan liposomes with folate, and the liposomes were characterized by particle size, entrapment efficiency, cytotoxicity to A549 cells and in vitro release profile. Technical evaluations were performed on lung cancer A549 cells and xenografted A549 cancer cells in female nude mice, and the pharmacokinetics of the drug were evaluated in female SD rats. Results: The folate-targeted topotecan liposomes were proven to show effectiveness in targeting lung tumors. The anti-tumor effects of these liposomes were demonstrated by the decreased tumor volume and improved therapeutic efficacy. The folate-targeted topotecan liposomes also lengthened the topotecan blood circulation time. Conclusion: The folate-targeted topotecan liposomes are effective drug delivery systems and can be easily modified with folate, enabling the targeted liposomes to deliver topotecan to lung cancer cells and kill them, which could be used as potential carriers for lung chemotherapy.

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Sevoflurane inhibits proliferation, invasion, but enhances apoptosis of lung cancer cells by Wnt/β-catenin signaling via regulating lncRNA PCAT6/ miR-326 axis

Open Life Sciences ◽

10.1515/biol-2020-0017 ◽

2020 ◽

Vol 15 (1) ◽

pp. 159-172

Author(s):

Guoning Su ◽

Zhibing Yan ◽

Min Deng

Keyword(s):

Lung Cancer ◽

Cancer Cells ◽

Volatile Anesthetic ◽

Lung Cancer Cells ◽

Luciferase Reporter ◽

Dependent Manner ◽

Luciferase Reporter Gene ◽

Western Blot Assay ◽

Gene Assay ◽

Cancer Tissues

AbstractSevoflurane was frequently used as a volatile anesthetic in cancer surgery. However, the potential mechanism of sevoflurane on lung cancer remains largely unclear. In this study, lung cancer cell lines (H446 and H1975) were treated by various concentrations of sevoflurane. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assessment and colony formation assay were performed to detect the cell viability and proliferation, separately. Also, transwell assay or flow cytometry assay was applied as well to evaluate the invasive ability or apoptosis in lung cancer cells, respectively. Western blot assay was employed to detect the protein levels of β-catenin and Wnt5a. Moreover, quantitative real-time polymerase chain reaction (qRT-PCR) was used to examine the expression level of prostate cancer-associated transcript 6 (PCAT6) and miR-326 in lung cancer tissues and cells. The target interaction between miR-326 and PCAT6 or Wnt5a was predicted by bioinformatics analysis and verified by the dual-luciferase reporter gene assay. Sevoflurane inhibited the abilities on viability, proliferation, invasion, and activation of Wnt/β-catenin signaling, but promoted apoptosis of H446 and H1975 cells in a dose-dependent manner. The expression of PCAT6 was increased in lung cancer tissues and cells, except for that of miR-326. Besides, sevoflurane could lead to expressed limitation of PCAT6 or improvement of miR-326. This process presented a stepwise manner. Up-regulation of PCAT6 restored the suppression of sevoflurane on abilities of proliferation, invasion, rather than apoptosis, and re-activated the Wnt5a/β-catenin signaling in cells. Moreover, the putative binding sites between miR-326 and PCTA6 or Wnt5a were predicted by starBase v2.0 software online. PCAT6 suppressing effects on cells could be reversed by pre-treatment with miR-326 vector. The promotion of Wnt5a inverted effects led from miR-326 or sevoflurane. Our study indicated that sevoflurane inhibited the proliferation, and invasion, but enhanced the apoptosis in lung cancer cells by regulating the lncRNA PCAT6/miR-326/Wnt5a/β-catenin axis.

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Ovalitenone Inhibits the Migration of Lung Cancer Cells via the Suppression of AKT/mTOR and Epithelial-to-Mesenchymal Transition

Molecules ◽

10.3390/molecules26030638 ◽

2021 ◽

Vol 26 (3) ◽

pp. 638

Author(s):

Kittipong Sanookpan ◽

Nongyao Nonpanya ◽

Boonchoo Sritularak ◽

Pithi Chanvorachote

Keyword(s):

Lung Cancer ◽

Cell Migration ◽

Cancer Cells ◽

Colony Formation ◽

Cancer Metastasis ◽

Epithelial To Mesenchymal Transition ◽

A549 Cells ◽

Lung Cancer Cells ◽

Migration And Invasion ◽

Mesenchymal Transition

Cancer metastasis is the major cause of about 90% of cancer deaths. As epithelial-to-mesenchymal transition (EMT) is known for potentiating metastasis, this study aimed to elucidate the effect of ovalitenone on the suppression of EMT and metastasis-related behaviors, including cell movement and growth under detached conditions, and cancer stem cells (CSCs), of lung cancer cells. Methods: Cell viability and cell proliferation were determined by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazo-liumbromide (MTT) and colony formation assays. Cell migration and invasion were analyzed using a wound-healing assay and Boyden chamber assay, respectively. Anchorage-independent cell growth was determined. Cell protrusions (filopodia) were detected by phalloidin-rhodamine staining. Cancer stem cell phenotypes were assessed by spheroid formation. The proteins involved in cell migration and EMT were evaluated by Western blot analysis and immunofluorescence staining. Results: Ovalitenone was used at concentrations of 0–200 μM. While it caused no cytotoxic effects on lung cancer H460 and A549 cells, ovalitenone significantly suppressed anchorage-independent growth, CSC-like phenotypes, colony formation, and the ability of the cancer to migrate and invade cells. The anti-migration activity was confirmed by the reduction of filopodia in the cells treated with ovalitenone. Interestingly, we found that ovalitenone could significantly decrease the levels of N-cadherin, snail, and slug, while it increased E-cadherin, indicating EMT suppression. Additionally, the regulatory signaling of focal adhesion kinase (FAK), ATP-dependent tyrosine kinase (AKT), the mammalian target of rapamycin (mTOR), and cell division cycle 42 (Cdc42) was suppressed by ovalitenone. Conclusions: The results suggest that ovalitenone suppresses EMT via suppression of the AKT/mTOR signaling pathway. In addition, ovalitenone exhibited potential for the suppression of CSC phenotypes. These data reveal the anti-metastasis potential of the compound and support the development of ovalitenone treatment for lung cancer therapy.

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Circular RNA FLNA acts as a sponge of miR-486-3p in promoting lung cancer progression via regulating XRCC1 and CYP1A1

Cancer Gene Therapy ◽

10.1038/s41417-021-00293-w ◽

2021 ◽

Author(s):

Jiongwei Pan ◽

Gang Huang ◽

Zhangyong Yin ◽

Xiaoping Cai ◽

Enhui Gong ◽

...

Keyword(s):

Lung Cancer ◽

Cancer Cells ◽

Cancer Cell ◽

Cancer Progression ◽

Lung Cancer Cells ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Related Factors

AbstractSignificantly high-expressed circFLNA has been found in various cancer cell lines, but not in lung cancer. Therefore, this study aimed to explore the role of circFLNA in the progression of lung cancer. The target gene of circFLNA was determined by bioinformatics and luciferase reporter assay. Viability, proliferation, migration, and invasion of the transfected cells were detected by CCK-8, colony formation, wound-healing, and transwell assays, respectively. A mouse subcutaneous xenotransplanted tumor model was established, and the expressions of circFLNA, miR-486-3p, XRCC1, CYP1A1, and related genes in the cancer cells and tissues were detected by RT-qPCR, Western blot, or immunohistochemistry. The current study found that miR-486-3p was low-expressed in lung cancer. MiR-486-3p, which has been found to target XRCC1 and CYP1A1, was regulated by circFLNA. CircFLNA was located in the cytoplasm and had a high expression in lung cancer cells. Cancer cell viability, proliferation, migration, and invasion were promoted by overexpressed circFLNA, XRCC1, and CYP1A1 but inhibited by miR-486-3p mimic and circFLNA knockdown. The weight of the xenotransplanted tumor was increased by circFLNA overexpression yet reduced by miR-486-3p mimic. Furthermore, miR-486-3p mimic reversed the effect of circFLNA overexpression on promoting lung cancer cells and tumors and regulating the expressions of miR-486-3p, XRCC1, CYP1A1, and metastasis/apoptosis/proliferation-related factors. However, overexpressed XRCC1 and CYP1A1 reversed the inhibitory effect of miR-486-3p mimic on cancer cells and tumors. In conclusion, circFLNA acted as a sponge of miR-486-3p to promote the proliferation, migration, and invasion of lung cancer cells in vitro and in vivo by regulating XRCC1 and CYP1A1.

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MiR-107 inhibits proliferation of lung cancer cells through regulating TP53 regulated inhibitor of apoptosis 1 (TRIAP1)

Open Life Sciences ◽

10.1515/biol-2017-0023 ◽

2017 ◽

Vol 12 (1) ◽

pp. 200-205 ◽

Cited By ~ 2

Author(s):

Bing Wang ◽

Zhanjie Zuo ◽

Fang Lv ◽

Liang Zhao ◽

Minjun Du ◽

...

Keyword(s):

Lung Cancer ◽

Cell Proliferation ◽

Western Blot ◽

Cancer Cells ◽

A549 Cells ◽

Lung Cancer Cells ◽

Pcr Analysis ◽

Aberrant Expression ◽

Small Interference Rna ◽

Qrt Pcr

AbstractAimsAccumulating evidence indicates that aberrant expression of miR-107 plays a crucial role in cancers. This study aims to display the function of miR-107 and its novel target genes in the progression of lung cancer.Methods and MaterialMiR-107 or miR-107 inhibitor was transfected into lung cancer cells A549. The levels of miR-107 and TP53 regulated inhibition of apoptosis 1 (TRIAP1) were examined by quantitative real-time Polymerase Chain Reaction (qRT-PCR) analysis and Western Blot. Functionally, MTT and colony formation assays were carried out to test the effect of miR-107 inhibitor and/or small interference RNA (siRNA) targeting TRIAP1 mRNA on proliferation of lung cancer cells. Levels of miR-107 or TRIAP1 were detected in clinical lung cancer samples by using qRT-PCR analysis.ResultsQRT-PCR analysis revealed that miR-107 inhibitor or miR-107 was successfully transfected into A549 cells. Western Blot indicated that miR-107 decreased the expression of TRIAP1 protein in the cells. In contrast, miR-107 inhibitor augmented the levels of TRIAP1 protein. Functionally, miR-107 inhibitor remarkably suppressed A549 cell proliferation, whereas, TRIAP1 siRNAs could abrogate the miR-107 inhibitor-induced proliferation of cells. Then, we validated that TRIAP1 was increased in clinical lung cancer samples. MiR-107 expression was negatively related to TRIAP1 expression in clinical lung cancer samples.ConclusionsMiR-107 suppresses cell proliferation by targeting TRIAP1 in lung cancer. Our finding allows new insights into the mechanisms of lung cancer that is mediated by miR-107.

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Long noncoding RNA LCAT1 functions as a ceRNA to regulate RAC1 function by sponging miR-4715-5p in lung cancer

Molecular Cancer ◽

10.1186/s12943-019-1107-y ◽

2019 ◽

Vol 18 (1) ◽

Cited By ~ 17

Author(s):

Juze Yang ◽

Qiongzi Qiu ◽

Xinyi Qian ◽

Jiani Yi ◽

Yiling Jiao ◽

...

Keyword(s):

Lung Cancer ◽

Cancer Cells ◽

Noncoding Rna ◽

Small Gtpase ◽

Lung Cancer Cells ◽

Luciferase Reporter ◽

Rna Seq ◽

Lung Carcinogenesis ◽

Cancer Tissues

Abstract Introduction Long noncoding RNAs (lncRNAs) are emerging as key players in the development and progression of cancer. However, the biological role and clinical significance of most lncRNAs in lung carcinogenesis remain unclear. In this study, we identified and explored the role of a novel lncRNA, lung cancer associated transcript 1 (LCAT1), in lung cancer. Methods We predicted and validated LCAT1 from RNA-sequencing (RNA-seq) data of lung cancer tissues. The LCAT1–miR-4715-5p–RAC1 axis was assessed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Signaling pathways altered by LCAT1 knockdown were identified using RNA-seq. Furthermore, the mechanism of LCAT1 was investigated using loss-of-function and gain-of-function assays in vivo and in vitro. Results LCAT1 is an oncogene that is significantly upregulated in lung cancer tissues and associated with poor prognosis. LCAT1 knockdown caused growth arrest and cell invasion in lung cancer cells in vitro, and inhibited tumorigenesis and metastasis in the mouse xenografts. Mechanistically, LCAT1 functions as a competing endogenous RNA for miR-4715-5p, thereby leading to the upregulation of the activity of its endogenous target, Rac family small GTPase 1 (RAC1). Moreover, EHop-016, a small molecule inhibitor of RAC1, as an adjuvant could improve the Taxol monotherapy against lung cancer cells in vitro. Conclusions LCAT1–miR-4715-5p–RAC1/PAK1 axis plays an important role in the progression of lung cancer. Our findings may provide valuable drug targets for treating lung cancer. The novel combination therapy of Taxol and EHop-016 for lung cancer warrants further investigation, especially in lung cancer patients with high LCAT1 expression.

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Propofol Inhibits Lung Cancer A549 Cell Growth and Epithelial‐Mesenchymal Transition Process by Upregulation of MicroRNA-1284

Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics ◽

10.3727/096504018x15172738893959 ◽

2018 ◽

Vol 27 (1) ◽

pp. 1-8 ◽

Cited By ~ 12

Author(s):

Wei-Zhen Liu ◽

Nian Liu

Keyword(s):

Lung Cancer ◽

Cell Viability ◽

Cancer Cells ◽

A549 Cell ◽

Epithelial Mesenchymal Transition ◽

A549 Cells ◽

Lung Cancer Cells ◽

Migration And Invasion ◽

Mesenchymal Transition ◽

Foxm1 Expression

Propofol has been widely used in lung cancer resections. Some studies have demonstrated that the effects of propofol might be mediated by microRNAs (miRNAs). This study aimed to investigate the effects and mechanisms of propofol on lung cancer cells by regulation of miR-1284. A549 cells were treated with different concentrations of propofol, while transfected with miR-1284 inhibitor, si-FOXM1, and their negative controls. Cell viability, migration, and invasion, and the expression of miR-1284, FOXM1, and epithelial‐mesenchymal transition (EMT) factors were detected by CCK-8, Transwell, qRT-PCR, and Western blot assays, respectively. In addition, the regulatory and binding relationships among propofol, miR-1284, and FOXM1 were assessed, respectively. Results showed that propofol suppressed A549 cell viability, migration, and invasion, upregulated E-cadherin, and downregulated N-cadherin, vimentin, and Snail expressions. Moreover, propofol significantly promoted the expression of miR-1284. miR-1284 suppression abolished propofol-induced decreases of cell viability, migration, and invasion, and increased FOXM1 expression and the luciferase activity of FOXM1-wt. Further, miR-1284 negatively regulated FOXM1 expression. FOXM1 knockdown reduced cell viability, migration, and invasion by propofol treatment plus miR-1284 suppression. In conclusion, our study indicated that propofol could inhibit cell viability, migration, invasion, and the EMT process in lung cancer cells by regulation of miR-1284.

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3,5-Dimethyaminophenol is not Mutagenic in Ames Test and HPRT Test and may have Anti-Carcinogenic Potential Against Lung Cancer Cells

Proceedings ◽

10.3390/proceedings2251553 ◽

2018 ◽

Vol 2 (25) ◽

pp. 1553

Author(s):

Ming-Wei Chao ◽

Chia-Yi Tseng ◽

Pei-Ying Lin ◽

Yu-Jung Chang ◽

Özge Köse ◽

...

Keyword(s):

Lung Cancer ◽

Salmonella Typhimurium ◽

Cancer Cells ◽

Cho Cells ◽

Ames Test ◽

A549 Cells ◽

Lung Cancer Cells ◽

Lung Fibroblasts ◽

Carcinogenic Potential

Exposure to 3,5-dimethylaminophenol (3,5-DMAP), the metabolite of the 3-5-dimethylaniline, was shown to cause high levels of oxidative stress in different cells. However, we have shown that this alkylaniline metabolite was non-mutagenic to different strains of Salmonella typhimurium in Ames test and also was found to be not mutagenic to CHO cells in HPRT test. Concerning all the available data, we aimed to observe whether this metabolite may have anti-carcinogenic potential in human non-small cell lung cancer line (A549 cells). 3,5-DMAP caused a dose-dependent increase in cytotoxicity and generation of superoxide (O2-.) and reactive oxygen species (ROS). 3,5-DMAP did not produce significant cytotoxicity to human lung fibroblasts even at very high concentrations; however showed higher cytotoxic effect on A549 lung cancer cells at the same concentrations. 3,5-DMAP also led to molecular events, like increases in apoptotic markers (i.e., p53, Bad, Bax and cytochrome and decreases anti-apoptotic proteins (Bcl-2). Furthermore, 3,5-DMAP provided significant decreases in cell viability of A549 cells and eventually inhibited growth of A549 cells in an in vivo mouse model. Tumor sections showed that 3,5-DMAP down-regulated c-Myc expression but up-regulated p53 and cytochrome c, all of which might result in tumor growth arrest. In conclusion, our findings demonstrate 3,5-DMAP is not mutagenic to Salmonella typhimurium and CHO cells; toxic to A549 cells and therefore may have anti-cancer properties, the importance of which should be elucidated with further mechanistic studies.

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