Next-Generation Sequencing Reveals the Role of Epigallocatechin-3-Gallate in Regulating Putative Novel and Known microRNAs Which Target the MAPK Pathway in Non-Small-Cell Lung Cancer A549 Cells

Bhardwaj, Vaishali; Mandal, Abul Kalam Azad

doi:10.3390/molecules24020368

Cited by 37 publications

(30 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…EGCG has been demonstrated to possess anticancer bioactivity, which has attracted attention; EGCG has demonstrated cancer preventive activity in various types of human cancer, including lung, oral cavity and esophageal cancers (37,38). Numerous studies have been conducted on the effects of EGCG on lung cancer (39)(40)(41)(42), and it had been reported that oral administration of EGCG was feasible and safe to patients with advanced lung cancer (43).…”

Section: Discussionmentioning

confidence: 99%

PTEN/AKT/mTOR signaling mediates anticancer effects of epigallocatechin‑3‑gallate in ovarian cancer

Qin

Wang

et al. 2020

Oncol Rep

View full text Add to dashboard Cite

Epigallocatechin-3-gallate (EGCG), a polyphenol present in green tea, exhibits anticancer effects in various types of cancer. A number of studies have focused on the effects of EGCG on lung cancer, but not ovarian cancer. Previous reports have implicated that EGCG suppressed ovarian cancer cell proliferation and induced apoptosis, but its potential anticancer mechanisms and signaling pathways remain unclear. Thus, it is necessary to determine the anti-ovarian cancer effects of EGCG and explore the underlying mechanisms. In the present study, EGCG exerted stronger proliferation inhibition on SKOV3 cells compared with A549 cells and induced apoptosis in SKOV3 cells, as well as upregulated PTEN expression and downregulated the expression of phosphoinositide-dependent kinase-1 (PDK1), phosphor (p)-AKT and p-mTOR. These effects were reversed by the PTEN inhibitor VO-Ohpic trihydrate. The results of the mouse xenograft experiment demonstrated that 50 mg/kg EGCG exhibited increased tumor growth inhibition compared with 5 mg/kg paclitaxel. In addition, PTEN expression was upregulated, whereas the expression levels of PDK1, p-AKT and p-mTOR were downregulated in the EGCG treatment group compared with those in untreated mice in vivo. In conclusion, the results of the present study provided a new underlying mechanism of the effect of EGCG on ovarian cancer and may lead to the development of EGCG as a candidate drug for ovarian cancer therapy.

show abstract

Section: Discussionmentioning

confidence: 99%

PTEN/AKT/mTOR signaling mediates anticancer effects of epigallocatechin‑3‑gallate in ovarian cancer

Qin

Wang

et al. 2020

Oncol Rep

View full text Add to dashboard Cite

show abstract

“…In addition, FXS-3 could activate the JNK signaling pathway but inhibit the ERK/p38 signaling pathways, which might be an important mechanism underlying the apoptosis of lung cancer cells induced by FXS-3. Recently, microRNAs play a significant role in the MAPK signaling cascade [9]. It will be interesting to explore the potential microRNAs modulated by FXS-3 in A549 cells.…”

Section: Discussionmentioning

confidence: 99%

A Ferulic Acid Derivative FXS-3 Inhibits Proliferation and Metastasis of Human Lung Cancer A549 Cells via Positive JNK Signaling Pathway and Negative ERK/p38, AKT/mTOR and MEK/ERK Signaling Pathways

et al. 2019

View full text Add to dashboard Cite

Lung cancer is one of the most common malignancies and is an increasing cause of cancer-related deaths. In our previous study, a series of ferulic acid (FA) derivatives were designed and synthesized; they exhibited positive anti-cancer activities, especially for a compound labelled FXS-3. In this study, a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was performed, wherein it revealed the inhibitory effect of FXS-3 on the proliferation and metastasis of human lung cancer A549 cells. The further flow cytometry assay showed that FXS-3 induced apoptosis of A549 cells induced cell cycle arrest at the G0/G1 phase. The trans-well migration and Matrigel invasion assays revealed that FXS-3 inhibited the migration and invasion of A549 cells. By the western blotting analysis, FXS-3 increased the expression of B-cell lymphoma-2 (Bcl-2) associated X protein (Bax)/Bcl-2 ratio, inhibited matrix metalloproteinase (MMP)-2 and MMP-9, and regulated the extracellular signal-regulated kinase (ERK)/p38, c-Jun N-terminal kinase (JNK), protein kinase B (AKT)/mechanistic target of rapamycin (mTOR), as well as mitogen-activated protein kinase (MEK)/ERK signaling pathways. The subsequent A549 xenograft-bearing mouse model and tail vein injection of A549 cells induced pulmonary tumor metastasis model showed that FXS-3 significantly restrained the tumor growth and metastasis. In conclusion, FXS-3 might inhibit proliferation and metastasis of human lung cancer A549 cells by positively regulating JNK signaling pathway and negativly regulating ERK/p38, AKT/mTOR, and MEK/ERK signaling pathways, which provides important scientific basis for the development of anti-cancer drugs about FA derivatives.

show abstract

“…For example, studies showed that lncRNAs are dysregulated after EGCG treatment in lung cancer, nasopharyngeal carcinoma, prostatic hyperplasia, osteoarthritis, etc [33][34][35] However, whether lncRNAs mediated the protective role of catechin, a kind of bioactive polyphenol that has a variety of pharmacological and biological properties and plays a protective role in MI/R injury, 14 against H/R-induced myocardial cell apoptosis or MI/R injury is largely unknown. For example, studies showed that lncRNAs are dysregulated after EGCG treatment in lung cancer, nasopharyngeal carcinoma, prostatic hyperplasia, osteoarthritis, etc [33][34][35] However, whether lncRNAs mediated the protective role of catechin, a kind of bioactive polyphenol that has a variety of pharmacological and biological properties and plays a protective role in MI/R injury, 14 against H/R-induced myocardial cell apoptosis or MI/R injury is largely unknown.…”

Section: Discussionmentioning

confidence: 99%

“…LncRNAs are the cellular responding molecules for bioactive polyphenol treatment in various diseases. For example, studies showed that lncRNAs are dysregulated after EGCG treatment in lung cancer, nasopharyngeal carcinoma, prostatic hyperplasia, osteoarthritis, etc [33][34][35] However, whether lncRNAs mediated the protective role of catechin, a kind of bioactive polyphenol that has a variety of pharmacological and biological properties and plays a protective role in MI/R injury, 14 against H/R-induced myocardial cell apoptosis or MI/R injury is largely unknown. In this study, we found that lncRNA MIAT expression was down-regulated after catechin treatment in myocardial Same as the transcriptional regulation of other genes, mounting evidence showed that the transcription of lncRNAs could be regulated by transcription factors at the transcriptional level under physiological and pathological conditions.…”

Section: Discussionmentioning

confidence: 99%

Catechin relieves hypoxia/reoxygenation‐induced myocardial cell apoptosis via down‐regulating lncRNA MIAT

Wei

et al. 2020

J Cellular Molecular Medi

View full text Add to dashboard Cite

Background Catechin protects heart from myocardial ischaemia/reperfusion (MI/R) injury. However, whether catechin inhibits H/R‐induced myocardial cell apoptosis is largely unknown. Objective This study aims to investigate the underlying mechanism of catechin in inhibiting the apoptosis of H/R‐induced myocardial cells. Methods LncRNA MIAT expression was detected by qRT‐PCR. Cell viability of H9C2 cells was detected using CCK‐8 assay. The apoptosis of H9C2 cells was detected by flow cytometry. The interaction between CREB and MIAT promoter regions was confirmed by dual‐luciferase reporter gene assay and ChIP assay. Results In MI/R rats, catechin improved heart function and down‐regulated lncRNA MIAT expression in myocardial tissue. In H/R‐induced H9C2 cells, catechin protected against cell apoptosis, and lncRNA MIAT overexpression attenuated this protective effect of catechin. We confirmed that transcription factor CREB could bind to MIAT promoter region, and catechin suppressed lncRNA MIAT expression through up‐regulating CREB. Catechin improved mitochondrial function and relieved apoptosis through promoting Akt/Gsk‐3β activation. In addition, MIAT inhibited Akt/Gsk‐3β activation and promoted cell apoptosis in H/R‐induced H9C2 cells. Finally, we found catechin promoted Akt/Gsk‐3β activation through inhibiting MIAT expression in H/R‐induced H9C2 cells. Conclusion Catechin relieved H/R‐induced myocardial cell apoptosis through regulating CREB/lncRNA MIAT/Akt/Gsk‐3β pathway.

show abstract

Next-Generation Sequencing Reveals the Role of Epigallocatechin-3-Gallate in Regulating Putative Novel and Known microRNAs Which Target the MAPK Pathway in Non-Small-Cell Lung Cancer A549 Cells

Cited by 37 publications

References 64 publications

PTEN/AKT/mTOR signaling mediates anticancer effects of epigallocatechin‑3‑gallate in ovarian cancer

PTEN/AKT/mTOR signaling mediates anticancer effects of epigallocatechin‑3‑gallate in ovarian cancer

A Ferulic Acid Derivative FXS-3 Inhibits Proliferation and Metastasis of Human Lung Cancer A549 Cells via Positive JNK Signaling Pathway and Negative ERK/p38, AKT/mTOR and MEK/ERK Signaling Pathways

Catechin relieves hypoxia/reoxygenation‐induced myocardial cell apoptosis via down‐regulating lncRNA MIAT

Contact Info

Product

Resources

About