Department Of Human Genetics And Molecular Medicine

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    Melittin: a possible regulator of cancer proliferation in preclinical cell culture and animal models
    (Springer Science and Business Media Deutschland GmbH, 2023-11-03T00:00:00) Haque, Shafiul; Hussain, Arif; Joshi, Hemant; Sharma, Ujjawal; Sharma, Bunty; Aggarwal, Diwakar; Rani, Isha; Ramniwas, Seema; Gupta, Madhu; Tuli, Hardeep Singh
    Background: Melittin is a water-soluble cationic peptide derived from bee venom that has been thoroughly studied for the cure of different cancers. However, the unwanted interactions of melittin produce hemolytic and cytotoxic effects that hinder their therapeutic applications. To overcome the shortcomings, numerous research groups have adopted different approaches, including conjugation with tumor-targeting proteins, gene therapy, and encapsulation in nanoparticles, to reduce the non-specific cytotoxic effects and potentiate their anti-cancerous activity. Purpose: This article aims to provide mechanistic insights into the chemopreventive activity of melittin and its nanoversion in combination with standard anti-cancer drugs for the treatment of cancer. Methods: We looked over the pertinent research on melittin's chemopreventive properties in online databases such as PubMed and Scopus. Conclusion: In the present article, the anti-cancerous effects of melittin on different cancers have been discussed very nicely, as have their possible mechanisms of action to act against different tumors. Besides, it interacts with different signal molecules that regulate the diverse pathways of cancerous cells, such as cell cycle arrest, apoptosis, metastasis, angiogenesis, and inflammation. We also discussed the recent progress in the synergistic combination of melittin with standard anti-cancer drugs and a nano-formulated version of melittin for targeted delivery to improve its anticancer potential. Graphical abstract: [Figure not available: see fulltext.] � 2023, The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.
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    Molecular mechanisms behind ROS regulation in cancer: A balancing act between augmented tumorigenesis and cell apoptosis
    (Springer Science and Business Media Deutschland GmbH, 2022-11-28T00:00:00) Tuli, Hardeep Singh; Kaur, Jagjit; Vashishth, Kanupriya; Sak, Katrin; Sharma, Ujjawal; Choudhary, Renuka; Behl, Tapan; Singh, Tejveer; Sharma, Sheetu; Saini, Adesh K.; Dhama, Kuldeep; Varol, Mehmet; Sethi, Gautam
    ROS include hydroxyl radicals (HO.), superoxide (O2.), and hydrogen peroxide (H2O2). ROS are typically produced under physiological conditions and play crucial roles in living organisms. It is known that ROS, which are created spontaneously by cells through aerobic metabolism in mitochondria, can have either a beneficial or detrimental influence on biological systems. Moderate levels of ROS can cause oxidative damage to proteins, DNA and lipids, which can aid in the pathogenesis of many disorders, including cancer. However, excessive concentrations of ROS can initiate programmed cell death in cancer. Presently, a variety of chemotherapeutic drugs and herbal agents are being investigated to induce ROS-mediated cell death in cancer. Therefore, preserving ROS homeostasis is essential for ensuring normal cell development and survival. On account of a significant association of ROS levels at various concentrations with carcinogenesis in a number of malignancies, further studies are needed to determine the underlying molecular mechanisms and develop the possibilities for intervening in these processes. � 2022, The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.