Integrated single-cell RNA-seq analysis reveals mitochondrial calcium signaling as a modulator of endothelial-to-mesenchymal transition.

Endothelial cells (ECs) are highly plastic, capable of differentiating into various cell types. Endothelial-to-mesenchymal transition (EndMT) is crucial during embryonic development and contributes substantially to vascular dysfunction in many cardiovascular diseases (CVDs). While targeting EndMT holds therapeutic promise, understanding its mechanisms and modulating its pathways remain challenging.

DLG1 functions upstream of SDCCAG3 and IFT20 to control ciliary targeting of polycystin-2.

Polarized vesicular trafficking directs specific receptors and ion channels to cilia, but the underlying mechanisms are poorly understood. Here we describe a role for DLG1, a core component of the Scribble polarity complex, in regulating ciliary protein trafficking in kidney epithelial cells. Conditional knockout of Dlg1 in mouse kidney causes ciliary elongation and cystogenesis, and cell-based proximity labeling proteomics and fluorescence microscopy show alterations in the ciliary proteome upon loss of DLG1.

DLG1 functions upstream of SDCCAG3 and IFT20 to control ciliary targeting of polycystin-2.

Polarized vesicular trafficking directs specific receptors and ion channels to cilia, but the underlying mechanisms are poorly understood. Here we describe a role for DLG1, a core component of the Scribble polarity complex, in regulating ciliary protein trafficking in kidney epithelial cells. Conditional knockout of in mouse kidney caused ciliary elongation and cystogenesis, and cell-based proximity labelling proteomics and fluorescence microscopy showed alterations in the ciliary proteome upon loss of DLG1.

Orai3 Calcium Channel Regulates Breast Cancer Cell Migration through Calcium-Dependent and -Independent Mechanisms.

Orai3 calcium (Ca) channels are implicated in multiple breast cancer processes, such as proliferation and survival as well as resistance to chemotherapy. However, their involvement in the breast cancer cell migration processes remains vague. In the present study, we exploited MDA-MB-231 and MDA-MB-231 BrM2 basal-like estrogen receptor-negative (ER) cell lines to assess the direct role of Orai3 in cell migration.

Ion channels as key partners of cytoskeleton in cancer disease.

Several processes occur during tumor development including changes in cell morphology, a reorganization of the expression and distribution of the cytoskeleton proteins as well as ion channels. If cytoskeleton proteins and ion channels have been widely investigated in understanding cancer mechanisms, the interaction between these two elements and the identification of the associated signaling pathways are only beginning to emerge. In this review, we summarize the work published over the past 15 years relating to the roles played by ion channels in these mechanisms of reorganization of the cellular morphology, essential to metastatic dissemination, both through the physical interactions with elements of the cytoskeleton and by intracellular signaling pathways involved.

Store-Independent Calcium Entry and Related Signaling Pathways in Breast Cancer.

Known as a key effector in breast cancer (BC) progression, calcium (Ca) is tightly regulated to maintain the desired concentration to fine-tune cell functions. Ca channels are the main actors among Ca transporters that control the intracellular Ca concentration in cells. It is well known that the basal Ca concentration is regulated by both store-dependent and independent Ca channels in BC development and progression.

Ion Channels: New Actors Playing in Chemotherapeutic Resistance.

In the battle against cancer cells, therapeutic modalities are drastically limited by intrinsic or acquired drug resistance. Resistance to therapy is not only common, but expected: if systemic agents used for cancer treatment are usually active at the beginning of therapy (i.e.