Methionine enkephalin (MENK) suppresses lung cancer by regulating the Bcl-2/Bax/caspase-3 signaling pathway and enhancing natural killer cell-driven tumor immunity

Zhang, Shuling; Liu, Ning; Ma, Mingxing; Huang, Hai; Handley, Mike; Bai, Xueli; Shan, Fengping

doi:10.1016/j.intimp.2021.107837

Cited by 27 publications

(15 citation statements)

References 44 publications

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“…In an experimental study, Zhang et al [ 33 ] showed that the regulation of the BCL2/BAX/caspase-3 pathway by methionine enkephalin induced the apoptosis of lung cancer cells. Therefore, the statin-mediated activation of apoptosis may be useful in blocking neoplastic spread [ 25 , 34 ].…”

Section: Effects Of Statins On Lung Cancer Molecular Pathwaysmentioning

confidence: 99%

Effect of Statins on Lung Cancer Molecular Pathways: A Possible Therapeutic Role

Marcianò¹,

Palleria

Casarella³

et al. 2022

Pharmaceuticals

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Lung cancer is a common neoplasm, usually treated through chemotherapy, radiotherapy and/or surgery. Both clinical and experimental studies on cancer cells suggest that some drugs (e.g., statins) have the potential to improve the prognosis of cancer. In fact, statins blocking the enzyme “hydroxy-3-methylglutaryl-coenzyme A reductase” exert pleiotropic effects on different genes involved in the pathogenesis of lung cancer. In this narrative review, we presented the experimental and clinical studies that evaluated the effects of statins on lung cancer and described data on the effectiveness and safety of these compounds. We also evaluated gender differences in the treatment of lung cancer to understand the possibility of personalized therapy based on the modulation of the mevalonate pathway. In conclusion, according to the literature data, statins exert multiple effects on lung cancer cells, even if the evidence for their use in clinical practice is lacking.

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Section: Effects Of Statins On Lung Cancer Molecular Pathwaysmentioning

confidence: 99%

Effect of Statins on Lung Cancer Molecular Pathways: A Possible Therapeutic Role

Marcianò¹,

Palleria

Casarella³

et al. 2022

Pharmaceuticals

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“…Lung cancer, a major malignancy, is the leading cause of cancer death worldwide 1 . Although many therapies, such as surgery, radiotherapy and chemotherapy, have been applied to treat lung cancer, the 5‐year survival rate remains low due to tumor invasion and metastasis as well as lack of effective biomarkers and targets 2 . Hence, exploring novel approaches for the diagnosis and treatment of lung cancer are urgently required.…”

Section: Introductionmentioning

confidence: 99%

Exosomal circDNER enhances paclitaxel resistance and tumorigenicity of lung cancer via targeting miR‐139‐5p/ITGB8

Zhu

Weng

et al. 2022

Thoracic Cancer

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Background: Circular RNAs (circRNAs) are regarded as vital regulatory factors in various cancers. However, the biological functions of circDNER in the paclitaxel (PTX) resistance of lung cancer remain largely unexplored. Methods: Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to analyze circDNER, miR-139-5p, and ITGB8. Cell proliferation was assessed via colony formation and MTT assays. Cell apoptosis was evaluated by flow cytometry. Western blot was performed to assess protein expression. The targeted interaction among circDNER, miR-139-5p, and ITGB8 were validated using dualluciferase reporter or RNA immunoprecipitation assays. Results: Inhibition of circDNER reduced IC50 of PTX, inhibited cell proliferation, invasion and migration, as well as promoted cell apoptosis in PTX-resistant lung cancer cells. Mechanistically, circDNER sponged miR-139-5p to upregulate ITGB8 expression. Overexpression of miR-139-5p reversed the biological functions mediated by circDNER in PTX-resistant lung cancer cells. MiR-139-5p overexpression suppressed PTX resistance and malignant behaviors of PTX-resistant lung cancer cells, with ITGB8 elevation rescued the impacts. Moreover, we demonstrated that circDNER was upregulated in plasma exosomes from lung cancer patients. The plasma exosomes derived from these patients are the key factors enhancing the migration and invasion potential of lung cancer cells. Conclusion:The circDNER mediated miR-139-5p/ITGB8 axis suppresses lung cancer progression. Our findings suggest that circDNER might act as a potential prognostic biomarker and therapeutic target for lung cancer treatment.

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“…Drug transporter-independent mechanisms also play a prominent role in the development of MDR in LC. An important superfamily of antiapoptotic proteins known as the B-cell lymphoma (Bcl-2) appear to be upregulated in LC, promoting cytotoxic resistance through the dysregulation of apoptosis in tumor cells [52][53][54]. In addition, mutations in the p53 transcriptional factors that regulate the expressions of numerous genetic materials have brought about considerable MDR in LC [55][56][57].…”

Section: Multidrug Resistancementioning

confidence: 99%

Nanomedicine Strategies for Management of Drug Resistance in Lung Cancer

Haider

Elsherbeny

Pittalà

et al. 2022

IJMS

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Lung cancer (LC) is one of the leading causes of cancer occurrence and mortality worldwide. Treatment of patients with advanced and metastatic LC presents a significant challenge, as malignant cells use different mechanisms to resist chemotherapy. Drug resistance (DR) is a complex process that occurs due to a variety of genetic and acquired factors. Identifying the mechanisms underlying DR in LC patients and possible therapeutic alternatives for more efficient therapy is a central goal of LC research. Advances in nanotechnology resulted in the development of targeted and multifunctional nanoscale drug constructs. The possible modulation of the components of nanomedicine, their surface functionalization, and the encapsulation of various active therapeutics provide promising tools to bypass crucial biological barriers. These attributes enhance the delivery of multiple therapeutic agents directly to the tumor microenvironment (TME), resulting in reversal of LC resistance to anticancer treatment. This review provides a broad framework for understanding the different molecular mechanisms of DR in lung cancer, presents novel nanomedicine therapeutics aimed at improving the efficacy of treatment of various forms of resistant LC; outlines current challenges in using nanotechnology for reversing DR; and discusses the future directions for the clinical application of nanomedicine in the management of LC resistance.

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Methionine enkephalin (MENK) suppresses lung cancer by regulating the Bcl-2/Bax/caspase-3 signaling pathway and enhancing natural killer cell-driven tumor immunity

Cited by 27 publications

References 44 publications

Effect of Statins on Lung Cancer Molecular Pathways: A Possible Therapeutic Role

Effect of Statins on Lung Cancer Molecular Pathways: A Possible Therapeutic Role

Exosomal circDNER enhances paclitaxel resistance and tumorigenicity of lung cancer via targeting miR‐139‐5p/ITGB8

Nanomedicine Strategies for Management of Drug Resistance in Lung Cancer

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