Cell Biology

Peer review is essential for maintaining the quality of published research, but this skill is often not explicitly taught to early career researchers (ECRs). Joint peer review with supervisors can both promote ECR professional growth and enhance review quality. We describe the advantages and best practices of joint peer review.

In Caenorhabditis elegans oocytes, meiotic spindle movement toward the cortex before anaphase depends on kinesin-1. A recent study by Aquino et al. uncovers a novel mechanism whereby the inward organelle packing driven by kinesin-1 excludes the spindle from the center, thereby causing it to be positioned near the cortex.

While alkylated mRNAs are known to activate ribosome quality control in the cytoplasm, how do cells deal with damaged RNAs in the nucleus? In their current work, Tsao et al. discover a new pathway of RNA damage repair and unexpectedly find that RNA alkylation can induce R-loops and DNA breaks.

Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta (PI3Kβ) is recognized for its role in cellular signaling as a lipid kinase. He and colleagues recently reported a non-canonical function of PI3Kβ where, under high glucose, it phosphorylates and activates O-GlcNAc transferase (OGT). This activation enhances ATP-citrate synthase (ACLY) O-GlcNAcylation, increasing acetyl-CoA production, fueling fatty acid metabolism and histone acetylation, and driving glioblastoma (GBM) growth.

Circulating tumor cells (CTCs), which have the heterogeneity and histological properties of the primary tumor and metastases, are shed from the primary tumor and/or metastatic lesions into the vasculature and initiate metastases at remote sites. In the clinic, CTCs are used extensively in liquid biopsies for early screening, diagnosis, treatment, and prognosis. Current research focuses on using CTC-derived models to study tumor heterogeneity and metastasis, with 3D organoids emerging as a promising tool in cancer research and precision oncology. However, isolating and enriching CTCs from blood remains challenging due to their scarcity, exacerbated by the lack of an optimized culture medium for CTC-derived organoids (CTCDOs). In this review, we summarize the origin, isolation, enrichment, culture, validation, and clinical application of CTCs and CTCDOs.

Voltage-gated sodium channels (VGSCs) are best known for their role in the generation and propagation of action potentials in neurons, muscle cells, and cardiac myocytes, which have traditionally been labeled as ‘excitable’. However, emerging evidence challenges this traditional perspective. It is now clear that VGSCs are also expressed in a broad spectrum of cells outside the neuromuscular realm, where they regulate diverse cellular functions. In this review, we summarize current knowledge on the expression, regulation, and function of VGSCs in non-neuromuscular cells, highlighting their contributions to physiological processes and pathological conditions. Dynamic expression patterns of VGSCs in different cell types, involvement of VGSCs in cellular functions, such as phagocytosis, motility, and cytokine release, and their potential as therapeutic targets for diseases that include inflammatory disorders, osteoarthritis (OA), and cancer, are discussed. This new understanding of VGSCs and their effects on cells outside the neuromuscular realm opens new avenues for research and therapeutic interventions.

Neutrophils have recently received increased attention in cancer because they contribute to all stages of cancer. Neutrophils are so far considered to have a short half-life. However, a growing body of literature has shown that tumor-associated neutrophils (TANs) acquire a prolonged lifespan. This review discusses recent work surrounding the mechanisms by which neutrophils can persist in the tumor microenvironment (TME). It also highlights different scenarios for therapeutic targeting of protumorigenic neutrophils, supporting the idea that, in tumors, inhibition of neutrophil recruitment is not sufficient because these cells can persist and remain hidden from current interventions. Hence, the elimination of long-lived neutrophils should be pursued to increase the efficacy of standard therapy.

Glycosylation is a complex co-translational and post-translational modification (PTM) in eukaryotes that utilizes glycosyltransferases to generate a vast array of glycoconjugate structures. Recent studies have highlighted the role of glycans in regulating essential molecular, cellular, tissue, organ, and systemic biological processes with significant implications for human diseases, particularly cancer. The metabolic reliance of cancer, spanning tumor initiation, disease progression, and resistance to therapy, necessitates a range of uniquely altered cellular metabolic pathways. In addition, the intricate interplay between cell-intrinsic and -extrinsic mechanisms is exemplified by the communication between cancer cells, cancer stem cells (CSCs), cancer-associated fibroblasts (CAFs), and immune cells within the tumor microenvironment (TME). In this review article, we explore how differential glycosylation in cancer influences the metabolism and stemness features alongside new avenues in glycobiology.

Mitochondria are signaling hubs that produce immunomodulatory metabolites during the immune response. In addition, mitochondria also facilitate the recruitment and anchoring of immune signaling complexes during infection. Evolutionary conserved signaling intermediate in toll (ECSIT) was initially described as a positive regulator of the transcription factor Nuclear factor kappa-light chain enhancer of activated B cells (NF-κB). More recently, ECSIT has emerged as a regulator of bacterial clearance, mitochondrial reactive oxygen species (mROS), and mitophagy. In addition, ECSIT has been identified as a control point in responding to viral infection and tumorigenesis. Notably, ECSIT loss in different models and cell types has been found to lead to enhanced tumorigenesis. Thus, ECSIT functions as a metabolic tumor suppressor and limits cancer pathogenesis. In this review, we highlight the key functions and crosstalk mechanisms that ECSIT bridges between cell metabolism and immunity and focus then on the antitumor role of ECSIT independent of immunity.