Although β-carotene is known for its anti-carcinogenic and antioxidant properties, a few recent epidemiological and experimental evidence show that at higher concentration it acts as pro-oxidant and induces cancer. Since the global burden of breast cancer exceeds all other types of cancer, and its incidence rates is also in increasing trend, the present study attempted to evaluate the anti-cancer molecular mechanism of β-carotene (at 1 µM concentration) isolated from Spinacia oleracea in human breast cancer (MCF-7) cells. The carotenoid was purified by open column chromatography and identified by LC-MS. The anti-proliferative effect of β-carotene at different concentrations was evaluated by WST-1 assay and the changes in cell morphology were examined by microscopic observation. The induction of apoptosis by β-carotene was observed by DAPI staining and colorimetric caspase-3 assay. The expression of cell survival, apoptotic, and antioxidant marker proteins was measured by western blot analysis. Purified β-carotene inhibited the viability of MCF-7 cells in a dose-dependent manner, which was well correlated with changes in cell morphology. Increased apoptotic cells were observed in β-carotene (1 µM)-treated cells. This apoptosis induction was associated with increased caspase-3 activity. The protein expression studies showed that β-carotene at 1 µM concentration effectively decreases the expression of the anti-apoptotic protein, Bcl-2 and PARP, and survival protein, NF-kB. It also inhibited the activation of intracellular growth signaling proteins, Akt and ERK1/2. The inhibition of Akt activation by β-carotene results in decreased phosphorylation of Bad. Further, it down-regulated antioxidant enzyme, SOD-2, and its transactivation factor (Nrf-2), and endoplasmic reticulum (ER) stress marker, XBP-1, at protein levels. These findings exhibit the key role of β-carotene even at a low physiological concentration in MCF-7 cells which further explains its predominant anti-cancer activity.

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Background Coronavirus disease-(COVID-19) is an infectious pandemic caused by SARS-CoV-2. SARS-CoV-2 main protease (M pro ) and spike protein are crucial for viral replication and transmission. Spike protein recognizes the human ACE2 receptor and transmits SARS-CoV-2 into the human body. Thus, M pro , spike protein, and ACE2 receptor act as appropriate targets for the development of therapeutics against SARS-CoV-2. Spices are traditionally known to have anti-viral and immune-boosting activities. Therefore, we investigated the possible use of selected spice bioactives against the potential targets of SARS-CoV-2 using computational analysis. Methods Molecular docking analysis was performed to analyze the binding efficiency of spice bioactives against SARS-CoV-2 target proteins along with the standard drugs. Drug-likeness properties of selected spice bioactives were investigated using Lipinski's rule of five and the SWISSADME database. Pharmacological properties such as ADME/T, biological functions, and toxicity were analyzed using ADMETlab, PASS-prediction, and ProTox-II servers, respectively. Results Out of forty-six spice bioactives screened, six bioactives have shown relatively better binding energies than the standard drugs and have a higher affinity with at least more than two targets of SARS-CoV-2. The selected bioactives were analyzed for their binding similarities with the standard drug, remdesivir, towards the targets of SARS-CoV-2. Selected spice bioactives have shown potential drug-likeness properties, with higher GI absorption rate, lower toxicity with pleiotropic biological roles. Conclusions Spice bioactives have the potential to bind with the specific targets involved in SARS-CoV-2 infection and transmission. Therefore, spice-based nutraceuticals can be developed for the prevention and treatment of COVID-19.

Breast cancer is the leading cause of cancer-related death among women. Recurrence of primary tumor and metastasis to distant body parts are major causes of breast cancer-associated mortality. The 5-year survival rate for women with metastatic breast cancer is only 25–30%. Breast cancer metastasis is a series of processes involved with EMT, invasion, loss of cell to cell adhesion, alteration in cell phenotype, extravasation, microenvironment of the tumor, and colonization to the secondary sites. Epigenetic modification is involved in the transformation of the distant stromal cell into a secondary tumor. LncRNAs, are one the key epigenetic modifiers, are the largest endogenous non-coding RNAs with approximate base-pair lengths from 200 nt to 100 kb. LncRNA plays a crucial role in breast cancer metastasis by sponging miRNA, by degrading or silencing specific mRNA, or else by targeting the enzymes and microprocessor subunits involved in the biogenesis of miRNA. LncRNA also alters the expression of several genes involved in breast cancer metastasis and modulating different cell signaling pathways. The goal of this review is to provide a better understanding of the role of lncRNA in the regulation of breast cancer metastasis. We also summarized some of the key lncRNAs that regulate the genes and signaling pathways involved in breast cancer invasion and metastasis.