Multitarget Effects of Cross-Cancer Melittin in Reversing Chemotherapy Resistance in Solid Tumors: Focus on Breast Cancer, Ovarian Cancer, and Non-Small Cell Lung Cancer

The drug resistance to chemotherapy is a major setback in the management of the solid tumor minimalizing the efficiency of the chemotherapy and the chances of recurrence. This is a significant challenge to cancer treatment because long-term treatment can only be successful with this resistance. Recent research indicates that one of the active polypeptides in the bee venom, Melittin has multi-target effects, which can even reverse drug resistance in various forms of cancer and this points to the use of Melittin as a combination therapy alongside other drugs. In this paper, Melittin showed specific cancer-selective effects on the three common solid tumors namely: breast cancer, ovarian cancer and non-small cell lung cancer. Melittin plays its functions in breast cancer through two of the most important signaling pathways EGFR/HER2 and PI3K/Akt. Melittin interferes with these signaling networks inhibiting the survival of breast cancer cells and can potentially delay tumor growth. Melittin in ovarian cancer has the ability to disturb the lipid section and energy metabolism of cancer cells. Melittin has two vital roles in a non small cell lung cancer (NSCLC), which contributes to its effectiveness as a therapeutic candidate. To begin with, it promotes the natural body processes of apoptosis, which simply initiate self-destruction process among cancer cells. Second, Melittin suppresses anti-death mediation pathways, including the occurrence of NF-Kb, the involvement of which is essential facilitating the survival of cancer cells and their further proliferation. These mechanisms combined, combine to render Melittin an important ally in the fight against chemotherapy resistance, which is one of the main issues in the treatment of solid tumors. In addition to highlighting the promise of Melittin in augmenting traditional chemotherapy, this study forms the basis of designing therapy combinations that target specifically chemotherapy resistance.