Identification and validation of calcium extrusion-related genes prognostic signature in colon adenocarcinoma.

Background: Disruptions in calcium homeostasis are associated with a wide range of diseases, and play a pivotal role in the development of cancer. However, the construction of prognostic models using calcium extrusion-related genes in colon adenocarcinoma (COAD) has not been well studied. We aimed to identify whether calcium extrusion-related genes serve as a potential prognostic biomarker in the COAD progression.

Synergistic anticancer effect by targeting CDK2 and EGFR-ERK signaling.

The EGFR-RAS-ERK pathway is one of the most important signaling cascades in cell survival, growth, and proliferation. Aberrant activation of this pathway is a common mechanism in various cancers. Here, we report that CDK2 is a novel regulator of the ERK pathway via USP37 deubiquitinase (DUB).

Clinical characteristics and prognostic nomograms of 12555 non-severe COVID-19 cases with Omicron infection in Shanghai.

Background: Omicron variant of the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has rapidly become a global threat to public health. Numerous asymptomatic and mild cases had been admitted in shelter hospitals to quickly win the fight against Omicron pandemic in Shanghai. However, little is known about influencing factors for deterioration and length of stay (LOS) in hospitals among these non-severe cases.

USP37 regulates DNA damage response through stabilizing and deubiquitinating BLM.

The human RecQ helicase BLM is involved in the DNA damage response, DNA metabolism, and genetic stability. Loss of function mutations in BLM cause the genetic instability/cancer predisposition syndrome Bloom syndrome. However, the molecular mechanism underlying the regulation of BLM in cancers remains largely elusive.

PDE2 Inhibits PKA-Mediated Phosphorylation of TFAM to Promote Mitochondrial Ca-Induced Colorectal Cancer Growth.

Growing evidence indicates that the dysregulation of mitochondrial calcium (Ca) plays a critical role in the growth of tumor cells, including colorectal cancer (CRC). However, the underling mechanism is not fully elucidated. In this study, the regulatory effects of mitochondrial Ca on phosphodiesterase 2 (PDE2)/cAMP/PKA axis and the phosphorylation of mitochondrial transcription factor A (TFAM) as well as the growth of CRC cells were systematically investigated both and Our findings demonstrated that MCU-induced mitochondrial Ca uptake activated mitochondrial PDE2 in CRC cells.

MCU-induced mitochondrial calcium uptake promotes mitochondrial biogenesis and colorectal cancer growth.

Mitochondrial calcium uniporter (MCU) has an important role in regulating mitochondrial calcium (Ca) homeostasis. Dysregulation of mitochondrial Ca homeostasis has been implicated in various cancers. However, it remains unclear whether MCU regulates mitochondrial Ca uptake to promote cell growth in colorectal cancer (CRC).

MCUR1 facilitates epithelial-mesenchymal transition and metastasis via the mitochondrial calcium dependent ROS/Nrf2/Notch pathway in hepatocellular carcinoma.

Background: Mitochondrial Ca plays a critical role in tumorigenesis, including cell proliferation and metastasis. Mitochondrial calcium uniporter regulator 1 (MCUR1) has been shown to be frequently upregulated in HCC and promote cancer cell survival. However, whether MCUR1 is involved in the metastasis of HCC and its underlying mechanisms remain unknown.

Positive feedback loop between mitochondrial fission and Notch signaling promotes survivin-mediated survival of TNBC cells.

Mitochondrial morphology is remodeled by continuous dynamic cycles of fission and fusion. Emerging data have shown that the disturbance of balance between mitochondrial fission and fusion is involved in the progression of several types of neoplasms. However, the status of mitochondrial dynamics and its potential biological roles in breast cancer (BC), particularly in triple negative BC (TNBC) are not fully clear.

TNFα induces Ca influx to accelerate extrinsic apoptosis in hepatocellular carcinoma cells.

Background: Tumor necrosis factor-α has been proven an effective anticancer agent in preclinical studies. However, the translation of TNFα from research to clinic has been blocked by significant systemic toxicity and limited efficacy at maximal tolerated dose, which need urgently to be solved.

Methods: The level of cytosolic Ca was assessed by Fura-2 in HCC cells.