miRNAs in the prognosis of triple-negative breast cancer: A review.

Triple-Negative Breast Cancer (TNBC) is a highly aggressive and invasive type of breast cancer (BC) with high mortality rate wherein effective target medicaments are lacking. It is a very heterogeneous group with several subtypes that account for 10-20% of cancer among women globally, being negative for three most important receptors (estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2)), with an early and high recurrence resulting in poor survival rate. Therefore, a more thorough knowledge on carcinogenesis of TNBC is required for the development of personalized treatment options. miRNAs can either promote or suppress tumorigenesis and have been linked to a number of features of cancer progression, including proliferation, metastasis, apoptosis, and epithelial-mesenchymal transition (EMT). Recent miRNA research shows that there is great potential for the development of novel biomarkers as they have emerged as drivers of tumorigenesis and provide opportunities to target various components involved in TNBC, thus helping to solve this difficult-to-treat disease. In this review, we summarize the most relevant miRNAs that play an essential role in TNBC biology. Their role with regard to molecular mechanisms underlying TNBC progression has been discussed, and their potential use as therapeutic or prognostic markers to unravel the intricacy of TNBC based on the pieces of evidence obtained from various works of literature has been briefly addressed.

Metallothionein or metallothionein like proteins and heavy metal toxicity in Oreochromis mossambicus (Peters).

Metallothioneins or metallothionein like proteins protect the biological system by encountering the influx of metal ions. These proteins are present in the contaminated as well as uncontaminated organisms. Studies show that the native metallothioneins or metallothionein like proteins of O. mossambicus is predominantly zinc bound. Increased influx of zinc causes a redistribution of this essential metal to other proteins requiring zinc as co-factor. Influx of mercury is encountered by the displacement of zinc bound to the protein and also by de novo of synthesis of metal binding proteins and subsequent binding of the incoming mercury. Data available show that "spill over" hypothesis is too simple to explain the mechanism of heavy metal toxicity.