Reactive oxygen species (ROS) are extremely reactive molecules produced during cellular metabolism, which play important roles in signaling and immune responses. Excessive ROS accumulation results in oxidative stress and cellular damage. As a result, autophagy (a cellular recycling process) is induced to overcome oxidative stress conditions by eliminating impaired cellular components. By selectively targeting and degrading dysfunctional mitochondria and peroxisomes through mitophagy and pexophagy, respectively, cells can effectively reduce ROS accumulation. Conversely, oxidative stress can disrupt autophagy, impairing protein aggregate clearance and thereby exacerbating ROS accumulation. In this review, we discuss the complex correlation between oxidative stress and autophagy, highlighting the mechanisms of regulation and their pathological implications. Additionally, we discuss the latest advances and challenges in developing autophagy-modulating therapies.

A significant challenge in cancer treatment is the rising problem of drug resistance that reduces the effectiveness of therapeutic strategies. Current knowledge shows that multiple mechanisms play a role in cancer drug resistance. Another mechanism that has gained attention is the alteration in sphingolipid trafficking and the dysregulation of its metabolism, which was reported to cause cancer-associated drug resistance. Sphingolipids are lipids containing sphingosine and have multiple roles, ranging from lipid raft formation, apoptosis, and cell signaling to immune cell trafficking. Recent studies show that in developing cancer cells, altered or dysregulated sphingolipids are associated with drug efflux and promote the survival of cancer cells by bypassing apoptosis. Upregulated levels of the glucosylceramide synthase (GCS), an enzyme that functions in sphingolipid metabolism, lead to the upregulated ABCB1 gene that induces drug efflux from the cancer cells. These bypass mechanisms make drugs that induce apoptosis in tumor cells ineffective. By highlighting the current findings, this review aims to provide a mechanism of drug resistance caused by the dysregulation of glucosylceramide synthase, sphingosine kinase, and acid ceramidase enzymes as possible therapeutic targets to enhance the effectiveness of the currently used chemotherapeutic agents.

Metformin is an antidiabetic drug with reported potential antiproliferative activity against different cancer types including breast cancer. However, the mechanism of action of how metformin can induce its antiproliferative activity is still unclear. Thus, the current study is a systematic review of the literature aiming to explore the reported antiproliferative mechanisms of metformin against breast cancer. The study included seventeen research articles that describe different mechanisms of action against breast cancer. While the majority of the studies confirm the antiproliferative potential of metformin, albeit at different potencies, there appear to be various mechanisms and factors that can influence this effect. There are a number of questions yet to be answered pertaining the use of metformin as an anti-cancer agent, warranting further investigation into this emerging area of research.

The endoplasmic reticulum (ER) is critical in aiding cells in ensuring that proteins are folded and processed correctly, particularly during stressful situations. ER oxidoreductin-1 alpha (ERO1α) is an enzyme that is responsible for the formation of disulfide bonds during protein folding, along with protein disulfide isomerase (PDI). This redox pathway is often highly upregulated in cancer cells, allowing tumors to survive harsh conditions such as hypoxia and nutrient deprivation. This review discusses the role of the ERO1α–PDI system in cancer development through the regulation of oxidative stress, redox homeostasis, and tumor plasticity. It further shows the therapeutic potential of interrupting the ERO1α–PDI axis, which could lead to protein misfolding; enhanced generation of reactive oxygen species (ROS); and, eventually, cancer cell death.

Aim: To map RN workload, staffing indicators, resident outcomes, workforce sustainability and nursing‐management context in nursing homes. Background: Staffing ratios and hours per resident day (HPRD) quantify staffing but not role complexity, interruptions, supervisory demands, resident acuity, continuity or work environment. Evaluation: Following JBI guidance and PRISMA‐ScR, five databases were searched using an RN‐specific strategy and updated on 4 September 2026. Following source‐level eligibility reassessment and reconciliation of the updated search, 20 studies meeting the RN‐specific resident‐outcome criteria formed the primary synthesis. Seven studies that did not meet these criteria but provided relevant workforce or nursing‐management evidence were retained as a separately labelled contextual evidence layer and excluded from the primary synthesis and PRISMA included‐study count. Primary studies underwent full data charting, whereas contextual studies underwent restricted extraction for interpretive purposes only. Key Issues: Evidence was predominantly observational. Greater RN availability and more favourable work environments were generally associated with better resident outcomes, although findings varied by outcome, timing, staffing configuration and organisational context. Conclusions: RN workload is multidimensional and cannot be reduced to staffing ratios alone. Current evidence does not establish a universal RN staffing threshold or support causal conclusions across nursing‐home settings. Implications for Nursing Management: Managers should interpret staffing metrics alongside resident acuity, staffing continuity, workload intensity, skill mix, agency use and work‐environment indicators.