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Summary Tuberculosis (TB) along with acquired immune deficiency syndrome and malaria rank among the top three fatal infectious diseases which pose threat to global public health, especially in middle and low income countries. TB caused by Mycobacterium tuberculosis (Mtb) is an airborne infectious disease and one‐third of the world's population gets infected with TB leading to nearly 1·6 million deaths annually. TB drugs are administered in different combinations of four first‐line drugs (rifampicin, isoniazid, pyrazinamide and ethambutol) which form the core of treatment regimens in the initial treatment phase of 6–9 months. Several reasons account for the failure of TB therapy such as (i) late diagnosis, (ii) lack of timely and proper administration of effective drugs, (iii) lower availability of less toxic, inexpensive and effective drugs, (iv) long treatment duration, (v) nonadherence to drug regimen and (vi) evolution of drug‐resistant TB strains. Drug‐resistant TB poses a significant challenge to TB therapy and control programs. In the background of worldwide emergence of 558 000 new TB cases with resistance to rifampicin in the year 2017 and of them, 82% becoming multidrug‐resistant TB (MDR‐TB), it is essential to continuously update the knowledge on the mechanisms and molecular basis for evolution of Mtb drug resistance. This narrative and traditional review summarizes the progress on the anti‐tubercular agents, their mode of action and drug resistance mechanisms in Mtb. The aim of this review is to provide recent updates on drug resistance mechanisms, newly developed/repurposed anti‐TB agents in pipeline and international recommendations to manage MDR‐TB. It is based on recent literature and WHO guidelines and aims to facilitate better understanding of drug resistance for effective TB therapy and clinical management.

The use of novel and improved chemopreventive and chemotherapeutic agents for the prevention and treatment of cancer is on the rise. Natural products have always afforded a rich source of such agents. Epidemiological evidence suggests that a higher flavonoid intake is associated with low cancer risk. Accumulating data clearly indicate that the induction of apoptosis is an important component in the chemoprevention of cancer by naturally occurring dietary agents. Resveratrol, a naturally occurring polyphenol, demonstrates pleiotropic health benefits, including antioxidant, anti-inflammatory, antiaging, cardioprotective, and neuroprotective activities. Because of these properties and their wide distribution throughout the plant kingdom, resveratrol is envisioned as a potential chemopreventive/curative agent. Currently, a number of preclinical findings from our lab and elsewhere suggest resveratrol to be a promising natural weapon in the war against cancer. Remarkable progress in elucidating the molecular mechanisms underlying the anticancer properties of resveratrol has been achieved. Here, we focus on some of the myriad pathways that resveratrol targets to exert its chemopreventive role and advocate that resveratrol holds tremendous potential as an efficient anticancer drug of the future.

De novo lipogenesis, a hallmark for cancers is required for cellular transformation. Further it is believed that resistance to apoptosis and epithelial-to-mesenchymal-transition(EMT) facilitates metastasis via over-expression of anti-apoptotic Bcl-2. Previously we demonstrated that hsa-miR-195 targets BCL2, induces apoptosis and augmented the effect of etoposide in breast cancer cells. However, the mechanism behind its function remains elusive. Herein gene expression profiling was done in presence/absence of hsa-miR-195 in Breast cancer cells. IPA revealed mitochondrial dysfunction, fatty acid metabolism and xenobiotic metabolism signalling among the top processes being affected. For the first time we herein identified ACACA, FASN (the key enzymes of de novo fatty acid synthesis), HMGCR (the key enzyme of de novo cholesterol synthesis) and CYP27B1 as direct targets of hsa-miR-195. We further showed that ectopic expression of hsa-miR-195 in MCF-7 and MDA-MB-231 cells not only altered cellular cholesterol and triglyceride levels significantly but also resulted in reduced proliferation, invasion and migration. We further demonstrated that over expression of hsa-miR-195 decreased the Mesenchymal markers expression and enhanced Epithelial markers. In conclusion we say that hsa-miR-195 targets the genes of de novo lipogenesis, inhibits cell proliferation, migration, and invasion which potentially opens new avenues for the treatment of breast cancer.