: A member of cathepsin enzymes called Cathepsin B, is a cysteine-protease enzyme that plays significant roles in metalloproteinase regulation. Cathepsin B stands out amidst other members of cathepsin because of its role in both normal body physiology and pathophysiology. Being an anti-apoptotic and a pro-apoptotic agent, Cathepsin B has been reported to have deleterious effects, especially when its expression, activities, and distribution are outrageous. The over-expression of cathepsin B is traceable to dysregulation of one or more regulated steps involved in its synthesis. Consequently, the over-expression of cathepsin B contributes to the pathogenesis of different types of cancers – a global menace. Interestingly, the synthesis of this enzyme has been reported to be inhibited by several metal compounds, thus, curbing its involvement in carcinogenesis. In this review, the synthesis, structure, localization, and roles of cathepsin B in carcinogenesis were explored. Likewise, we also discussed the capacity of metallic compounds to inhibit this enzyme. Metals such as gold, ruthenium, palladium, Iridium, and Tellurium demonstrated remarkable activity toward cathepsin B of different modes. A relationship between cytotoxicity and inhibition constants was observed.

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Zoonotic diseases occur as a result of human interactions with animals with the inadvertent transmission of pathogens from one to another. Zoonoses remain a major cause of morbidity and mortality among human populations, as they have been a source of pandemics in human history. Viral zoonoses account for a significant percentage of pathogens of zoonotic sources, posing a huge risk to men’s general health and fertility. This review identifies the existing knowledge on the effects of viral zoonotic diseases on male fertility. Evidence from reviewed articles showed that viral zoonotic diseases elicit an immune reaction that induces inflammatory mediators and impairs testicular functions such as spermatogenesis and steroidogenesis, leading to abnormal semen parameters that lead to subfertility/infertility. Although most zoonotic viruses linger in semen long after recovery, their presence in semen does not directly translate to sexual transmission. There is a need to further delineate the possible risk of the sexual transmission of these diseases. While a few of the viral zoonotic diseases discussed have been well-studied, there is a need to place attention on others so as to fully understand their effects on male reproduction and therefore take the right steps towards preserving male fertility.

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Triple-negative breast cancer (TNBC), characterized by a deficiency in estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor2 (HER2), is among the most lethal subtypes of breast cancer (BC). Nevertheless, the molecular determinants that contribute to its malignant phenotypes such as tumor heterogeneity and therapy resistance, remain elusive. In this study, we sought to identify the stemness-associated genes involved in TNBC progression. Using bioinformatics approaches, we found 55 up- and 9 downregulated genes in TNBC. Out of the 55 upregulated genes, a 5 gene-signature (CDK1, EZH2, CCNB1, CCNA2, and AURKA) involved in cell regeneration was positively correlated with the status of tumor hypoxia and clustered with stemness-associated genes, as recognized by Parametric Gene Set Enrichment Analysis (PGSEA). Enhanced infiltration of immunosuppressive cells was also positively correlated with the expression of these five genes. Moreover, our experiments showed that depletion of the transcriptional co-factor nucleus accumbens-associated protein 1 (NAC1), which is highly expressed in TNBC, reduced the expression of these genes. Thus, the five genes signature identified by this study warrants further exploration as a potential new biomarker of TNBC heterogeneity/stemness characterized by high hypoxia, stemness enrichment, and immune-suppressive tumor microenvironment.