Cancer is a global health problem associated with genetics and unhealthy lifestyles. Increasingly, pathogenic infections have also been identified as contributors to human cancer initiation and progression. Most pathogens (bacteria, viruses, fungi, and parasites) associated with human cancers are categorized as Group I human carcinogens by the International Agency for Research on Cancer, IARC. These pathogens cause carcinogenesis via three known mechanisms: persistent infection that cause inflammation and DNA damage, initiation of oncogene expression, and immunosuppression activity of the host. In this review, we discuss the carcinogenesis mechanism of ten pathogens, their implications, and some future considerations for better management of the disease. The pathogens and cancers described are Helicobacter pylori (gastric cancer), Epstein-Barr virus (gastric cancer and lymphoma), Hepatitis B and C viruses (liver cancer), Aspergillus spp. (liver cancer), Opisthorchis viverrine (bile duct cancer), Clonorchis sinensis (bile duct cancer), Fusobacterium nucleatum (colorectal cancer), Schistosoma haematobium (bladder cancer); Human Papillomavirus (cervical cancer), and Kaposi’s Sarcoma Herpes Virus (Kaposi’s sarcoma).

Zinc oxide nanoparticles (ZnO-NPs) in their many formulations have prompted an immense interest in nanomedicine and drug development. Numerous ZnO-NPs bioactive formulations demonstrate remarkable broad applications in deciphering their therapeutic effects and bioimaging. Their unique size, morphology-dependent properties and modifiable surface chemistry have made them promising candidates for translation into novel, alternative nanomedicines. ZnO-NPs demonstrate biocompatibility and are non-toxic with relatively required in-expensive production techniques. This review presents an in-depth comprehension of the synthesis, chemical and biological peculiarities of ZnO-NPs, including their varied manufacturing methods and their impactful applications in biomedicine. The physical, chemical and biological synthesis approaches that are unique for ZnO-NPs synthesis were comprehensively reviewed, followed by their applications in therapeutics (anticancer, antibacterial, drug delivery, skin treatment, antidiabetic and antioxidant), diagnostics (bioimaging and biosensor) and theranostics as well as their health hazards. ZnO-NPs exhibit antibacterial and anticancer activities, primarily through the liberation of zinc ions and generation of reactive oxygen species (ROS), which disrupt the cell membrane. Their anticancer properties are additionally apprised with an escalation in caspase 3/7 along with the modulation of pro- and anti-apoptotic proteins. ZnO-NPs are reviewed to attenuate hepatocellular carcinoma. Further, this article comprehended various in-vitro and in-vivo therapeutic effects of novel drug formulations of ZnO-NPs. It also delved into two fascinating areas: ZnO-NPs’ performance in comparison with other NPs and the potential of ZnO-NPs heterostructures with 2D nanomaterials. The goal of this review is to inspire further research efforts to meet the growing needs of next-generation nanomedicine.

The gut microbiota Parvimonas micra has been found to be enriched in gut mucosal tissues and fecal samples of colorectal cancer (CRC) patients compared to non-CRC controls. In this study, we investigated the tumorigenic potential of P. micra and its regulatory pathways in CRC using HT-29, a low-grade CRC intestinal epithelial cell. For every P. micra-HT-29 interaction assay, HT-29 was co-cultured anaerobically with P. micra at an MOI of 100:1 (bacteria: cells) for 2 hr. We found that P. micra increased HT-29 cell proliferation by 38.45% (P=0.008), with the highest wound healing rate at 24 hr post-infection (P=0.02). In addition, inflammatory marker expression (IL-5, IL-8, CCL20, CSF2) was also significantlyinduced. Shotgun proteomics profiling analysis revealed that P. micra affects the protein expression of HT-29 (157 up-regulated; 214 down-regulated proteins). Upregulation of PSMB4 protein and its neighbouring subunits revealed association of the ubiquitin-proteasome pathway in CRC carcinogenesis; whereas downregulation of CUL1, YWHAH, and MCM3 signified cell cycle dysregulation. Moreover, 22 clinically relevant epithelial-mesenchymal transition (EMT)-markers were expressed in HT-29 infected with P. micra. Overall, this study elucidated exacerbated oncogenic properties of P. micra in HT-29 via aberrant cell proliferation, enhanced wound healing, inflammation, upregulation of ubiquitin-proteasome pathway (UPPs) and activation of EMT pathways.

Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype that is often associated with a poorer prognosis and does not respond to hormonal therapy. Increasing evidence highlights the exploitability of Annexin A1 (AnxA1), a calcium dependent protein, as a precision medicine for TNBC. To systematically summarize the role of AnxA1 and its associated mechanisms in TNBC, we performed data mining using three main databases: PubMed, Scopus, and Ovid/Medline. The papers retrieved were based on two different sets of key words such as “Annexin A1” or “Lipocortin 1” and “Breast cancer” or “TNBC”. A total of 388 articles were identified, with 210 chosen for comprehensive screening and 13 papers that met inclusion criteria were included. Current evidence from cell culture studies showed that AnxA1 expression is correlated with NF-κB, which promotes migration by activating ERK phosphorylation. AnxaA1 also activates TGF-β signaling which upregulates MMP-9 and miR196a expression to enhance epithelial-mesenchymal transition and migratory capacity of TNBC cells. AnxA1 can steer the macrophage polarization toward the M2 phenotype to create a pro-tumor immune environment. Existing research suggests a potential role of AnxA1 in the metastasis and immune landscape of TNBC tumors. Preclinical and clinical experiments are warranted to investigate the feasibility and effectiveness of targeting AnxA1 in TNBC.

Breast cancer treatments leads to variable responses. Hormonal therapy is beneficial to receptor positive breast cancersubtypes and display better clinical outcome than triple negative breast cancers (TNBCs) with FEC (5-Fluorouracil,Epirubicin and Cyclophosphamide) the mainstay chemotherapy regiment. Owning to their negative expressions ofestrogen (ER), progesterone (PR) and HER2 receptors, disease recurrence and metastasis befalls some patients indicatingresistance to FEC. Involvement of epigenetic silencing through DNA methylation, histone methylation, acetylation andsumoylation may be the key player in FEC chemoresistance. Epigenetic and molecular profiling successfully classifiedbreast cancer subtypes, indicating potential driver mechanisms to the progression of TNBCs but functional mechanismsbehind chemoresistance of these molecular markers are not well defined. Several epigenetic inhibitors and drugs havebeen used in the management of cancers but these attempts are mainly beneficial in hematopoietic cancers and notspecifically favourable in solid tumours. Hypothetically, upon administration of epigenetic drugs, recovery of tumoursuppressor genes is expected. However, high tendency of switching on global metastatic genes is predicted. Polycombrepressive complex (PRC) such as EZH2, SETD1A, DNMT, is known to have repressive effects in gene regulation andshown to inhibit cell proliferation and invasion in breast cancers. Individual epigenetic regulators may be an optionto improve chemo-drug delivery in cancers. This review discussed on molecular signatures of various breast cancersubtypes and on-going attempts in understanding underlying molecular mechanisms of epigenetic regulators as wellas providing insights on possible ways to utilize epigenetic enzymes/inhibitors with responses to chemotherapeuticdrugs to re-program cellular and biological outcome in TNBCs.