Cervical cancer ranks as the fourth most common cancer among women globally, posing a significant mortality risk. Persistent infection with high-risk human papillomavirus (HPV) is the primary instigator of cervical cancer development, often alongside coinfection with other viruses, precipitating various malignancies. This study aimed to explore recent biotechnological advances in understanding HPV infection dynamics, host interactions, and its role in oncogenesis. The gathered data shed light on HPV biology, host-virus interplay, viral coinfections, and cellular transformations leading to HPV-associated cancers. Recent years have seen the introduction of diverse vaccination strategies, including live attenuated, subunit, and DNA-based vaccines, complemented by innovative nanotechnology and plant-based products. Despite rich data addressing research inquiries, urgent calls echo for the implementation of contemporary screening and therapeutic modalities at clinical levels. Moreover, extensive public awareness campaigns are imperative to alleviate the burden of HPV-related diseases, emphasizing the necessity for proactive intervention strategies in combating this global health challenge.

Cancers are worldwide health concerns, whether they are sporadic or hereditary. The fundamental mechanism that causes somatic or oncogenic mutations and ultimately aids cancer development is still unknown. However, mammalian cells with protein-only somatic inheritance may also contribute to cancerous malignancies. Emerging data from a recent study show that prion-like proteins and prions (PrP^C) are crucial entities that have a functional role in developing neurological disorders and cancer. Furthermore, excessive PrP^C expression profiling has also been detected in non-neuronal tissues, such as the lymphoid cells, kidney, GIT, lung, muscle, and mammary glands. PrP^C expression is strongly linked with the proliferation and metastasis of pancreatic, prostate, colorectal, and breast malignancies. Similarly, experimental investigation presented that the PrP^C expression, including the prion protein-coding gene (PRNP) and p53 ag are directly associated with tumorigenicity and metastasis (tumor suppressor gene). The ERK2 (extracellular signal-regulated kinase) pathway also confers a robust metastatic capability for PrP^C-induced epithelial to mesenchymal transition. Additionally, prions could alter the epigenetic regulation of genes and overactive the mitogen-activated protein kinase (MAPK) signaling pathway, which promotes the development of cancer in humans. Protein overexpression or suppression caused by a prion and prion-like proteins has also been linked to oncogenesis and metastasis. Meanwhile, additional studies have discovered resistance to therapeutic targets, highlighting the significance of protein expression levels as potential diagnostic indicators and therapeutic targets.

This review highlights the pivotal roles of autophagy, ferroptosis, and endoplasmic reticulum (ER) stress in mediating cadmium (Cd)-induced nephrotoxicity. Cadmium exposure results in ER stress, which in turn activates major UPR pathways such as IRE1, ATF6, and PERK. By encouraging lipid peroxidation and suppressing cellular antioxidant defence, these mechanisms worsen ferroptosis and produce a feedback mechanism that increases cellular damage. There are two roles of autophagy in Cd-induced ferroptosis, which include its action in reducing cadmium-induced cytotoxicity by breaking down damaged components, and excessive autophagy, namely ferritinophagy, which promotes ferroptosis by iron dysregulation. The rise of mitochondrial ROS (MitoROS) caused by Cd-induced mitochondrial malfunction aids ferroptosis. This, in turn, causes ER stress and autophagy. This implies that focusing on mitochondrial health could be a useful treatment strategy. Effective treatment approaches include autophagy inhibitors like chloroquine, which have been shown to effectively reduce Cd-induced ferroptosis, and promising medicines that suppress ER stress, such as TUDCA. Desferrioxamine and other iron chelators effectively lower lipid peroxidation and iron dysregulation, therefore preventing ferroptotic cell death. Additionally, a multi-targeted treatment plan is suggested that targets iron metabolism, ER stress, and autophagy. In order to create tailored treatments for Cd-induced nephrotoxicity, this review emphasizes the need for additional study into the molecular pathways of Cd-induced ferroptosis, namely the ER stress-autophagy axis. The goal of future research should be to apply these mechanistic insights to clinical settings to enhance public health outcomes and create efficient therapies for renal failure brought on by cadmium toxicity.