Breast cancer is a type of cancer that originates in the cells of the breast tissues. B. pinnatum, C. sieberiana, C. tora and T. indica are the four medicinal plants whose phytochemicals were used for this In silico study. In this study, eight different ligands were evaluated for their interactions with the human epidermal growth factor 2 (HER2) protein (PDB ID: 3pp0). The ligands, including Apigenin, Bryophyllin A, Catechin, Emodin, Islandicin, Quercetin, Sitosterol, and Taxifolin, were assessed based on binding scores and hydrogen bond interactions. Among these ligands, Apigenin exhibited the highest binding score (- 6.5 kcal/mol), indicating its strong binding affinity to the HER2 protein. Bryophyllin A also displayed a significant binding score (- 6.3 kcal/mol) and formed a hydrogen bond with Met 901. Catechin, while having a slightly lower binding score (- 5.9 kcal/mol), engaged in hydrogen bonds with Ser 728, Arg 849, and Asn 850. Emodin, Quercetin, and Taxifolin demonstrated moderate binding scores (- 6.2, – 6.4, and – 6.0 kcal/mol, respectively) and formed hydrogen bonds with Asp 863 and Met 801. Islandicin formed a hydrogen bond with Gly 787 and Leu 786, with a binding score of – 6.1 kcal/mol. Sitosterol exhibited the lowest binding score (- 5.3 kcal/mol) but still established a hydrogen bond with Asp 863 and Met 801. Overall, Apigenin and Bryophyllin A emerged as the most promising ligands due to their strong binding affinities and specific hydrogen bond interactions with HER2. However, experimental validation is essential to confirm these findings and explore their potential as inhibitors or modulators of HER2. Furthermore, all ligands were successfully docked to the active sites of the HER2 protein, indicating their potential relevance in targeting HER2-related pathways. Importantly, the ligands exhibited favorable pharmacokinetic properties with no violations, except for Sitosterol, which showed minor violations in Lipinski, Ghose, Egan, and Muegge’s rules.
Breast cancer is a type of cancer that originates in the cells of the breast tissues. It primarily affects women but can also occur in men. It is characterized by the uncontrolled growth of abnormal cells in the breast tissue, forming a lump or mass called a tumor (Dashti et al., 2020). Breast cancer can spread to other parts of the body through the lymphatic system or bloodstream, leading to metastasis (Iqbal and Iqbal, 2014; Pegram and Jackisch, 2023). Early detection and advancements in treatment have significantly improved the prognosis and survival rates for those diagnosed with breast cancer (Pegram and Jackisch, 2023). The exact causes of breast cancer are not fully understood, but several risk factors have been identified. These include genetics (family history of breast cancer or carrying certain mutations like BRCA1 and BRCA2), hormonal factors (early onset of menstruation, late menopause, hormone replacement therapy), age (risk increases with age), certain inherited gene mutations, exposure to ionizing radiation, obesity, alcohol consumption, and more (Sun et al., 2017). While these factors can increase the risk, not everyone with these risk factors will develop breast cancer. Breast cancer can have wide-ranging effects on individuals physically, emotionally, and socially. Physically, it can lead to symptoms such as a lump in the breast, changes in breast size or shape, skin changes, and nipple discharge (Kim, 2021; Sun et al., 2017). Emotionally, the diagnosis can cause anxiety, fear, depression, and uncertainty. Socially, it may impact relationships and daily life. The effects of treatment, including surgery, chemotherapy, radiation, and hormone therapy, can also cause physical and emotional challenges. Treatment for breast cancer depends on the stage and type of cancer, as well as individual factors (Iqbal and Iqbal, 2014; Pegram and Jackisch, 2023). Common treatments include surgery (lumpectomy or mastectomy), radiation therapy, chemotherapy, targeted therapy, hormone therapy, and immunotherapy (Burguin and Diorio, 2021; Moo et al., 2019). Treatment plans may involve a combination of these approaches (Pegram and Jackisch, 2023). The goal is to remove or destroy the cancer cells, prevent recurrence, and improve overall quality of life (Moo et al., 2019). Researchers have identified specific molecular and genetic targets that play a role in the development and growth of breast cancer. Targeted therapies focus on these specific molecules, receptors, and genetic mutations to inhibit cancer growth (Burguin and Diorio, 2021). Some targeted therapies are designed to block hormone receptors (such as estrogen or progesterone receptors), while others target overexpressed proteins like HER2. HER2, or human epidermal growth factor receptor 2, is a protein that plays a role in regulating cell growth and division. In some breast cancers, there is an overexpression or amplification of the HER2 gene, leading to an increased production of the HER2 protein (Hussain et al., 2020; Iqbal and Iqbal, 2014). HER2-positive breast cancer is an important target in breast cancer treatment because the overexpression of HER2 is associated with more aggressive tumor growth and a poorer prognosis (Iqbal and Iqbal, 2014). Targeting HER2 can help slow down the progression of the cancer and improve treatment outcomes. In molecular docking studies, the HER2 (human epidermal growth factor receptor 2)
