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Background:: The carcinogenesis of uterine cervix is predominantly initiated with the consistent infection of human papilloma virus (HPV). Owing to the adverse side effects of standard chemotherapeutics in the treatment of recurrent and metastatic cervical cancer, there is a need for better and effective treatment modality. In this lieu of concern, natural compounds have proven their worthwhile potential against treatment of various carcinomas. Carvacrol is a phenolic monoterpenoid and several reports have suggested its different biological properties including antioxidant, anti-inflammatory and anticancer activity. Objective:: The objective of our present study was to investigate the effect of carvacrol on HPV18+ HeLa cervical cancer cells. Methods:: HeLa cervical cancer cells were cultured and subsequently treated with various doses of carvacrol. Cell viability was assessed via MTT assay. DAPI and Hoechst3342 staining was used to qualitatively analyzed the induced apoptosis. Reactive Oxygen Species (ROS) was estimated by DCFDA staining protocol and quantitatively estimated by flow cytometry. The cell cycle distribution and apoptosis (FITC-Annexin V assay) were analyzed by flow cytometry. Results:: The results of the present study have established that carvacrol strongly suppresses proliferation of cervical cancer cells via caspase-dependent apoptosis and abrogation of cell cycle progression. Furthermore, our preliminary study also demonstrated that carvacrol exhibits synergistic effect with chemotherapeutic drugs (5-FU and carboplatin). These initial findings implicated that natural compounds could reduce the toxic effects of chemotherapeutic drugs. Conclusion:: Therefore, this investigation affirms the anti-cancer potential of carvacrol against cervical cancer cells which could be an appendage in the prevention and treatment of cervical cancer.

Globally, cancer is one of the deadliest diseases, estimated to cause 9.9 million deaths in 2020. Conventional cancer treatments commonly involve mono‐chemotherapy or a combination of radiotherapy and mono‐chemotherapy. However, the negative side effects of these approaches have been extensively reported and have prompted the search for new therapeutic drugs. Over the past few years, numerous dietary agents, medicinal plants, and their phytochemicals gained considerable therapeutic importance because of their anticancer, antiviral, anti‐inflammatory, and antioxidant activities. Recent years have shown that essential oils possess therapeutic effects against numerous cancers. They are primarily used due to their lesser side effects than standard chemotherapeutic drugs. Carvacrol (CRV) is a phenolic monoterpenoid found in essential oils of oregano, thyme, pepperwort, wild bergamot, and other plants. Numerous anticancer reports of CRV substantiated that the main mechanistic action of CRV involves reduction in the viability of cancer cells and induction of apoptosis via both intrinsic and extrinsic pathways. CRV also obstructs the migration and invasion of cells leading to the suppressed proliferation rate. Furthermore, CRV mediates augmented ROS generation resulting in DNA damage and also halts the progression of cell cycle. Treatment of CRV modulates the expression of apoptotic proteins (Bax, Bad) and molecular targets of various signaling pathways (PI3K/AKT/mTOR, MAPKs, and Notch) in multiple solid carcinomas. Hence, this review aimed to acquire and disseminate the knowledge of chemopreventive and anticancer effects of CRV and the mechanisms of action already described for the compound against numerous cancers, including solid carcinomas, to guide future research. Practical applications Development and formulation of phytocompound based anticancer drug agents to counteract the aftereffects of chemotherapeutic drugs is a propitious approach. CRV is a monoterpenoid consisting of a phenolic group obtained from the essential oils of oregano and thyme. These plants are being used as food flavoring spice and as fragrance ingredient in various cosmetic formulations. For the use of CRV as an efficient chemopreventive agent, different therapeutic interactions of CRV along with its targeted pathways and molecules, involved in the regulation of onset and progression of various types of solid carcinomas, need to be studied and explored thoroughly.

Lung carcinoma is the leading cause of cancer-related mortalities worldwide, and present therapeutical interventions are not successful enough to treat this disease in many cases. Recent years have witnessed a surge in exploring natural compounds for their antiproliferative efficacy to expedite the characterization of novel anticancer chemotherapeutics. Swertia chirayita is a valued medicinal herb and possess intrinsic pharmaceutical potential. However, elucidation of its anticancer effects at molecular levels remains unclear and needs to be investigated. We assessed the anticancer and apoptotic efficacy of S . chirayita ethanolic extract ( Sw -EtOH) on non-small cell lung cancer (NSCLC) A549 cells during this exploratory study. The results elucidated that S. chirayita extract induced toxic effects within lung cancer cells by ~1 fold during cytotoxicity and LDH release assay at a 400 μg/ml concentration. Sw -EtOH extract elevates the level of ROS, resulting in the disruption of Δψm and release of cytosolic cytochrome c by 3.15 fold. Activation of caspases-3, -8 & -9 also escalated by ~1 fold, which further catalyze the augmentation of PARP cleavage (~3 folds), resulting in a four-fold increase in Sw -EtOH induced apoptosis. The gene expression analysis further demonstrated that Sw -EtOH extracts inhibited JAK1/STAT3 signaling pathway by down-regulating the levels of JAK1 and STAT3 to nearly half a fold. Treatment of Sw -EtOH modulates the expression level of various STAT3 associated proteins, including Bcl-XL, Bcl-2, Mcl-1, Bax, p53, Fas, Fas-L, cyclinD1, c-myc, IL-6, p21 and p27 in NSCLC cells. Thus, our study provided a strong impetus that Sw -EtOH holds the translational potential of being further evaluated as efficient cancer therapeutics and a preventive agent for the management of NSCLC.