Trilobatin, an Active Dihydrochalcone from <i>Lithocarpus polystachyus</i>, Prevents Cisplatin-Induced Nephrotoxicity via Mitogen-Activated Protein Kinase Pathway-Mediated Apoptosis in Mice

Duan, Yue-yang; Mi, Xiao-jie; Su, Wenying; Tang, Shan; Jiang, Shuang; Wang, Zi; Zhao, Lichun; Li, Wei

doi:10.1021/acsomega.2c04142

Cited by 3 publications

(3 citation statements)

References 43 publications

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“…23,[24][25] These results suggest that nicotine may be necessary for HDAC1 carcinogenic contentmediated advanced development or chemotherapy treatment failure in lung cancer. 26 The intricate relationship between nicotine, HDAC1, and cisplatin resistance carries significant therapeutic implications.…”

Section: Discussionmentioning

confidence: 99%

Cisplatin‐resistance induces lung squamous carcinoma cell growth by nicotine‐mediated α7nAchR/HDAC1/Cyclin D1/pRb cell cycle activation

Rao,

Guo,

2024

Cell Biochemistry & Function

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The majority of adenocarcinoma lung cancer is found in nonsmokers. A history of tobacco use is more common in squamous cell carcinoma of the lung. The aim of this study is to identify the cisplatin (CDDP)‐resistance that promotes lung squamous carcinoma cell growth through nicotine‐mediated HDAC1/7nAchR/E2F/pRb cell cycle activation. Squamous cell carcinoma (NCI‐H520 and NCI‐H157) cells were examined after cisplatin and nicotine treatment by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐2H‐tetrazolium bromide assay, cell migration assay, immunofluorescence staining, western blot analysis, and immunoprecipitation analysis. Consequently, CDDP is released from DNA and Rb phosphorylated pRb as a result of nicotine‐induced cancer cell proliferation through 7nAchR, which then triggers the opening of the HDAC1 cell cycle. The cell cycle is stopped when CDDP adducts are present. Nicotine exerts cancer cytoprotective effects by allowing HDAC1 repair mechanisms to re‐establish E2F promoting DNA stimulation cell cycle integrity in the cytosol and preventing potential CDDP and HDAC1 suppressed in the nuclear. Concentration expression of nicotine causes squamous carcinoma cell carcinogens to emerge from inflammation. COX2, NF‐KB, and NOS2 increase as a result of nicotine‐induced squamous carcinoma cell inflammation. Nicotine enhanced the cell growth‐related proteins such as α7nAchR, EGFR, HDAC1, Cyclin D, Cyclin E, E2F, Rb, and pRb by western blot analysis. It also induced cancer cell inflammation and growth. As a result, we suggest that nicotine will increase the therapeutic resistance effects of CDDP. This has the potential to interact with nicotine through α7nAchR receptors and HDAC1/Cyclin D/E2F/pRb potentially resulting in CDDP therapy resistance, as well as cell cycle‐induced cancer cell growth.

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Section: Discussionmentioning

confidence: 99%

Cisplatin‐resistance induces lung squamous carcinoma cell growth by nicotine‐mediated α7nAchR/HDAC1/Cyclin D1/pRb cell cycle activation

Rao,

Guo,

2024

Cell Biochemistry & Function

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“…Li et al investigated trilobatin anticancer efficacy in gefitinib-resistant lung cancer cells [ 203 ]. Trilobatin (phloretin-4-O-glucoside) is a dihydrochalcone glucoside and derivative of phloretin found in the stems, leaves, flowers and fruits of apple plants [ 204 , 205 ]. Trilobatin has been detected in the leaves of Vitis species , in Lithocarpus polystachyus , and in different Malus species including Malus domestica and Malus trilobata .…”

Section: Cd133 As a Target In Cancer Therapiesmentioning

confidence: 99%

Unmasking the Deceptive Nature of Cancer Stem Cells: The Role of CD133 in Revealing Their Secrets

Pospieszna,

Dams-Kozlowska,

Udomsak

et al. 2023

IJMS

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Cancer remains a leading cause of death globally, and its complexity poses a significant challenge to effective treatment. Cancer stem cells and their markers have become key players in tumor growth and progression. CD133, a marker in various cancer types, is an active research area as a potential therapeutic target. This article explores the role of CD133 in cancer treatment, beginning with an overview of cancer statistics and an explanation of cancer stem cells and their markers. The rise of CD133 is discussed, including its structure, functions, and occurrence in different cancer types. Furthermore, the article covers CD133 as a therapeutic target, focusing on gene therapy, immunotherapy, and approaches to affect CD133 expression. Nanoparticles such as gold nanoparticles and nanoliposomes are also discussed in the context of CD133-targeted therapy. In conclusion, CD133 is a promising therapeutic target for cancer treatment. As research in this area progresses, it is hoped that CD133-targeted therapies will offer new and effective treatment options for cancer patients in the future.

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“…Cisplatin (CDDP), used for the treatment of malignancies has been of high efficacy during chemotherapeutic management of cancer but with the efficiency, several side effects which include nephrotoxicity have been reported [47,48]. With this, it is necessary to consider drugs that will protect the kidney from toxicity since ultrafiltration is primarily carried out by the kidney.…”

Section: Synergistic Effect Of Synthetic and Natural Product Drugsmentioning

confidence: 99%

Traditional Knowledge of Cancer Treatment in Southwestern Nigeria: An Ethnopharmacological Review

Akinwumi,

Ambali

2023

JCSN

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Alkyd resin from seed oil extract of Hura crepitans (sand box) have been prepared and evaluated for industrial application. The oil extracted was physicochemically characterized using Association of Official Analytical Chemists (AOAC) standard methods. The analytical data obtained are as follows: Iodine Value; 170.43g I2/100g, Saponification Value; 235.15mgKOH/g, Acid Value; 3.10mgKOH/g, Free fatty acid Value; 10mg/g, Moisture Content; 0.06%, Specific Gravity; 0.92g/m, and Refractive Index; 1.47. Epoxidation of fatty acids in the seed oil extract was confirmed via Fourier Transform Infrared Spectrometry (FTIR). The alkyd resin was prepared via a one-pot process using alcoholysis-polyesterification reaction. Resin evaluation showed that: the drying time was 24 hours; it was soluble in acetone, methanol, ethanol and toluene; acid value was 6.50 after 180minutes; for chemical resistance it was observed that no effect on the prepared resin after 18hours and on immersion in 3M NaoH a total removal of the resin was observed after 24 hours. This infers that the prepared resin is a drying oil which makes it suitable for use in varnishes, paints, soap and other allied production.

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Trilobatin, an Active Dihydrochalcone from Lithocarpus polystachyus, Prevents Cisplatin-Induced Nephrotoxicity via Mitogen-Activated Protein Kinase Pathway-Mediated Apoptosis in Mice

Cited by 3 publications

References 43 publications

Cisplatin‐resistance induces lung squamous carcinoma cell growth by nicotine‐mediated α7nAchR/HDAC1/Cyclin D1/pRb cell cycle activation

Cisplatin‐resistance induces lung squamous carcinoma cell growth by nicotine‐mediated α7nAchR/HDAC1/Cyclin D1/pRb cell cycle activation

Unmasking the Deceptive Nature of Cancer Stem Cells: The Role of CD133 in Revealing Their Secrets

Traditional Knowledge of Cancer Treatment in Southwestern Nigeria: An Ethnopharmacological Review

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