Journal of Cell Communication and Signaling最新文献

Papillary thyroid carcinoma (PTC), the most common thyroid cancer, has been linked to various molecular alterations. This study focuses on microRNA-223-3p, whose upregulated expression in PTC tissues appears to enhance tumor growth and cellular dysfunctions. Our findings demonstrate that microRNA-223-3p significantly promotes cell proliferation, invasion, and migration and induces epithelial-mesenchymal transition (EMT). Additionally, neurofibromatosis type 2 (NF2) is identified as a direct target, suggesting that microRNA-223-3p could be crucial in PTC pathogenesis and may offer a target for therapeutic intervention.

Chemo-resistance in ovarian cancer is currently a major obstacle to the treatment and recovery of ovarian cancer. Therefore, identifying factors associated with chemo-resistance in ovarian cancer may reverse chemo-sensitization. Using isobaric tags for relative and absolute quantitation (ITRAQ) technology, we found a small molecule peptide with annexin 1 (ANXA1) as a precursor protein. Then, we explored the effects and mechanisms of this small molecule peptide on the proliferation, apoptosis, and drug resistance of ovarian cancer resistant cells through CCK-8, EdU cell proliferation assay, Annexin V-FITC/PI assay, Western blot,qRT-PCR. ANXA114-26 was highly expressed in the serums of sensitive patients. ANXA114-26 promoted apoptosis of ovarian cancer cells and increased the sensitization of ovarian cancer cells to cisplatin. The ANXA114-26 and ANXA1 competitively bind formyl peptide receptors (FPR). ANXA114-26 decreased multidrug resistance-associated protein 1 (MRP1) expression in ovarian cancer cells through the FPR/Cyclin D1/NF-ĸBp65 pathway. We found a peptide derived named ANXA114-26 in the serum of ovarian cancer patients. It can reduce ovarian cancer cell proliferation and reduce MRP1 expression through the FPR/Cyclin D1/NF-ĸBp65 pathway.

Skeletal muscles undergo self-repair upon injury, owing to the resident muscle stem cells and their extensive communication with the microenvironment of injured muscles. Cytokines play a critical role in orchestrating intercell communication to ensure successful regeneration. Immune cells as well as other types of cells in the injury site, including muscle stem cells, are known to secret cytokines. However, the extent to which various cell types express distinct cytokines and how the secreted cytokines are involved in intercell communication during regeneration are largely unknown. Here we integrated 15 publicly available single-cell RNA-sequencing (scRNA-seq) datasets of mouse skeletal muscles at early regeneration timepoints (0, 2, 5, and 7 days after injury). The resulting dataset was analyzed for the expression of 393 annotated mouse cytokines. We found widespread and dynamic cytokine expression by all cell types in the regenerating muscle. Interrogating the integrated dataset using CellChat revealed extensive, bidirectional cell–cell communications during regeneration. Our findings provide a comprehensive view of cytokine signaling in the regenerating muscle, which can guide future studies of ligand-receptor signaling and cell–cell interaction to achieve new mechanistic insights into the regulation of muscle regeneration.

A mounting body of evidence suggests that the endoplasmic reticulum stress and the unfolded protein response are involved in the underlying mechanisms responsible for vascular diseases. Inositol-requiring protein 1α (IRE1α), the most ancient branch among the UPR-related signaling pathways, can possess both serine/threonine kinase and endoribonuclease (RNase) activity and can perform physiological and pathological functions. The IRE1α-signaling pathway plays a critical role in the pathology of various vascular diseases. In this review, we provide a general overview of the physiological function of IRE1α and its pathophysiological role in vascular diseases.

The endoplasmic reticulum (ER) is crucial for maintaining calcium balance, lipid biosynthesis, and protein folding. Disruptions in ER homeostasis, often due to the accumulation of misfolded or unfolded proteins, lead to ER stress, which plays a significant role in various diseases, especially cancer. Urological cancers, which account for high male mortality worldwide, pose a persistent challenge due to their incurability and tendency to develop drug resistance. Among the numerous dysregulated biological mechanisms, ER stress is a key factor in the progression and treatment response of these cancers. This review highlights the dual role of aberrant ER stress activation in urologic cancers, affecting both tumor growth and therapeutic outcomes. While ER stress can support tumor growth through pro-survival autophagy, it primarily inhibits cancer progression via apoptosis and pro-death autophagy. Interestingly, ER stress can paradoxically aid cancer progression through mechanisms such as exosome-mediated immune evasion. Additionally, the review examines how pharmacological interventions, particularly with phytochemicals, can stimulate ER stress-mediated tumor suppression. Key regulators, including PERK, IRE1α, and ATF6, are discussed for their roles in upregulating CHOP levels and triggering apoptosis. In conclusion, a deeper understanding of ER stress in urological cancers not only clarifies the complex interactions between cellular stress and cancer progression but also provides new opportunities for innovative therapeutic strategies.

Li, S., Li, S., Gao, Z. and Liu, Y. (2024), LncRNA HOTTIP promotes LPS-induced lung epithelial cell injury by recruiting DNMT1 to epigenetically regulate SP-C. J. Cell Commun. Signal, 18: e12020. https://doi.org/10.1002/ccs3.12020.

In the originally published article, the funding number was omitted. The correct sentence is:

The research was sponsored by the Scientific Research Project of Heilongjiang Health Commission (No. 2020-332).

We apologize for this error.

In vascular smooth muscle cells (VSMCs) and vascular endothelial cells (VECs), phosphatidylinositol 4,5-bisphosphate (PIP₂) acts as a substrate for phospholipase C (PLC)- and phosphoinositol 3-kinase (PI3K)-mediated signaling pathways and an unmodified ligand at ion channels and other macromolecules, which are key processes in the regulation of cell physiological and pathological phenotypes. It is envisaged that these distinct roles of PIP₂ are achieved by PIP₂-binding proteins, which act as PIP₂ buffers to produce discrete pools of PIP₂ that permits targeted release within the cell. This review discusses evidence for the expression, cell distribution, and role of myristoylated alanine-rich C-kinase substrate (MARCKS), a PIP₂-binding protein, in cellular signaling and function of VSMCs. The review indicates the possibilities for MARCKS as a therapeutic target for vascular disease involving dysfunctional cell proliferation and migration, endothelial barrier permeability, and vascular contractility such as atherosclerosis, systemic and pulmonary hypertension, and sepsis.