In most cases, cancer develops due to abnormal cell growth and subsequent tumour formation. Due to significant constraints with current treatments, natural compounds are being explored as potential alternatives. There are now around 30 natural compounds under clinical trials for the treatment of cancer. Tulsi, or Holy Basil, of the genus Ocimum, is one of the most widely available and cost-effective medicinal plants. In India, the tulsi plant has deep religious and medicinal significance. Tulsi essential oil contains a valuable source of bioactive compounds, such as camphor, eucalyptol, eugenol, alpha-bisabolene, beta-bisabolene, and beta-caryophyllene. These compounds are proposed to be responsible for the antimicrobial properties of the leaf extracts. The anticancer effects of tulsi (Ocimum sanctum L.) have earned it the title of “queen of herbs” and “Elixir of Life” in Ayurvedic treatment. Tulsi leaves, which have high concentrations of eugenol, have been shown to have anticancer properties. In a various cancers, eugenol exerts its antitumour effects through a number of different mechanisms. In light of this, the current review focuses on the anticancer benefits of tulsi and its primary phytoconstituent, eugenol, as apotential therapeutic agent against a wide range of cancer types. In recent years, tulsi has gained popularity due to its anticancer properties. In ongoing clinical trials, a number of tulsi plant compounds are being evaluated for their potential anticancer effects. This article discusses anticancer, chemopreventive, and antioxidant effects of tulsi.
Lung cancer is the leading cause of mortality from cancer worldwide. Lung adenocarcinoma (LUAD) is a type of non-small cell lung cancer (NSCLC) with highest prevalence. Kinesins a class of motor proteins are shown to be involved in carcinogenesis. We conducted expression, stage plot and survival analyses on kinesin superfamily (KIF) and scrutinized the key prognostic kinesins. Genomic alterations of these kinesins were studied thereafter via cBioPortal. A protein–protein interaction network (PPIN) of selected kinesins and 50 closest altering genes was constructed followed by gene ontology (GO) term and pathway enrichment analyses. Multivariate survival analysis based on CpG methylation of selected kinesins was performed. Lastly, we conducted tumor immune infiltration analysis. Our results found KIF11/15/18B/20A/2C/4A/C1 to be significantly upregulated and correlated with poor survival in LUAD patients. These genes also showed to be highly associated with cell cycle. Out of our seven selected kinesins, KIFC1 showed the highest genomic alteration with highest number of CpG methylation. Also, CpG island (CGI) cg24827036 was discovered to be linked to LUAD prognosis. Therefore, we deduced that reducing the expression of KIFC1 could be a feasible treatment strategy and that it can be a wonderful individual prognostic biomarker. CGI cg24827036 can also be used as a therapy site in addition to being a great prognostic biomarker.
Malaria is a vector-borne parasitic disease caused by the apicomplexan protozoan parasite Plasmodium. Malaria is a significant health problem and the leading cause of socioeconomic losses in developing countries. WHO approved several antimalarials in the last 2 decades, but the growing resistance against the available drugs has worsened the scenario. Drug resistance and diversity among Plasmodium strains hinder the path of eradicating malaria leading to the use of new technologies and strategies to develop effective vaccines and drugs. A timely and accurate diagnosis is crucial for any disease, including malaria. The available diagnostic methods for malaria include microscopy, RDT, PCR, and non-invasive diagnosis. Recently, there have been several developments in detecting malaria, with improvements leading to achieving an accurate, quick, cost-effective, and non-invasive diagnostic tool for malaria. Several vaccine candidates with new methods and antigens are under investigation and moving forward to be considered for clinical trials. This article concisely reviews basic malaria biology, the parasite's life cycle, approved drugs, vaccine candidates, and available diagnostic approaches. It emphasizes new avenues of therapeutics for malaria. Graphical Abstract
Background: SARS-CoV-2 emerged in late 2019, causes COVID-19. Patients treated with Zyesami were found to be 3-fold decrease in respiratory failure and improvement in clinical outcome. It was reported that Zyesami inhibits RNA replication of SARS-CoV-2, including several non-structural proteins that essential in viral RNA replication. SARS-CoV-2 is a distinctive virus that required nsp10 and nsp16 for its methyltransferases activity which is crucial for RNA stability and protein synthesis. Objective: Objective We aimed the in silico determination of inhibitory consequences of Zyesami on the SARS-CoV-2 nsp10/nsp16 complex. Targeting SARS-CoV-2 nsp10/ nsp16 protein complex may be used for the development of drug against the COVID-19. Methods: I-TASSER was used for secondary structure prediction of Zyesami. CABS-dock was used for modelling of Zyesami with SARS-CoV-2 nsp16 interaction. The docked complex was visualized using PyMol. The quality of the docking model was checked by using ProQdock. Results: The 3D structure of SARS-CoV 2, nsp10/nsp16 showed that essential interactions exist between nsp10 and nsp16. Significant contact areas of Zyesami exist across amino acid residues of nsp10; Asn40-Thr47, Val57-Pro59, Gly69-Ser72, Cys77-Pro84, Lys93-Tyr96. In addition, polar contacts between nsp16 and Zyesami are Asn299-Ser440, Val297-Asn443, Gly149-Tyr437, Gln159-Lys430, Asn178-Arg429, Ser146-Arg429, Ser146-Arg429, Lys147-Arg429, Asr221-Thr422, Lys183-Asp423, Lys183-Asp423, and Gln219-Asp423 the residues are shown of nsp16 and Zyesami respectively. Conclusion: Conclusion The structural bioinformatics analyses have indicated the potential binding specificity of Zyesami and nsp16. Data predict how the initial binding of Zyesami with nsp10 and nsp16 may occur. Moreover, this binding could significantly inhibit the 2 -O-MTase activity of the SARS-CoV nsp10/16 complex.
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