HSP90 C-terminal domain inhibition promotes VDAC1 oligomerization via decreasing K274 mono-ubiquitination in Hepatocellular Carcinoma.

Voltage-dependent anion-selective channel protein 1 (VDAC1) is the most abundant protein in the mitochondrial outer membrane and plays a crucial role in the control of hepatocellular carcinoma (HCC) progress. Our previous research found that cytosolic molecular chaperone heat shock protein 90 (Hsp90) interacted with VDAC1, but the effect of the C-terminal and N-terminal domains of Hsp90 on the formation of VDAC1 oligomers is unclear. In this study, we focused on the effect of the C-terminal domain of Hsp90 on VDAC1 oligomerization, ubiquitination, and VDAC1 channel activity.

Stanniocalcin 1 promotes lung metastasis of breast cancer by enhancing EGFR-ERK-S100A4 signaling.

Lung metastasis is the leading cause of breast cancer-related death. The tumor microenvironment contributes to the metastatic colonization of tumor cells in the lungs. Tumor secretory factors are important mediators for the adaptation of cancer cells to foreign microenvironments.

Amino Acid Leaching of Critical Metals from Spent Lithium-Ion Batteries Followed by Selective Recovery of Cobalt Using Aqueous Biphasic System.

To reduce the exploitation of mine resources and decrease the harm to the environment caused by urban electronic wastes, the recovery of critical metals in secondary resources is crucial. In this study, we have successfully developed an eco-friendly process to integrate the leaching and separation of cobalt (Co) from a spent lithium-ion battery (LIB) cathode using an amino acid-based aqueous biphasic system (ABS). We, for the first time, demonstrated a simple method for leaching a LIB cathode using only amino acids.

MCU-dependent negative sorting of miR-4488 to extracellular vesicles enhances angiogenesis and promotes breast cancer metastatic colonization.

Based on Stephen Paget's well-established theory, both cell-autonomous and non-cell-autonomous mechanisms are crucial for metastasis. Although the mitochondrial calcium uniporter (MCU) has been suggested to be involved in breast cancer (BC) progression via cell-autonomous mechanisms, whether it assists the metastasis of BC cells through non-cell-autonomous mechanisms remains unclear. This study aimed to demonstrate that the MCU regulates BC metastatic colonization via non-cell-autonomous mechanisms.

Calcium-sensing stromal interaction molecule 2 upregulates nuclear factor of activated T cells 1 and transforming growth factor-β signaling to promote breast cancer metastasis.

Background: Stromal interaction molecule (STIM) 2 is a key calcium-sensing molecule that regulates the stabilization of calcium ions (Ca) and therefore regulates downstream Ca-associated signaling and cellular events. We hypothesized that STIM2 regulates epithelial-mesenchymal transition (EMT) to promote breast cancer metastasis.

Methods: We determined the effects of gain, loss, and rescue of STIM2 on cellular motility, levels of EMT-related proteins, and secretion of transforming growth factor-β (TGF-β).

Knockdown of FAM64A suppresses proliferation and migration of breast cancer cells.

Background: FAM64A is a mitotic regulator promoting cell metaphase-anaphase transition, and it is frequently reported to be highly expressed in cancer cells. However, the role of FAM64A in human breast cancer (BrC) is poorly studied.

Methods: The expression of FAM64A mRNA in BrC samples was determined by RT-qPCR assay and TCGA database mining.

Highly selective and sensitive probes for the detection of Cr(vi) in aqueous solutions using diglycolic acid-functionalized Au nanoparticles.

In this study, a variety of diglycolic acid-functionalized gold nanoparticle (Au NP) probes are reported, which are highly sensitive for the detection of chromium ions, Cr(vi) ions, at low concentrations in aqueous solutions based on the application of surface plasmon resonance (SPR) theory. Due to its outstanding affinity for Cr(vi) ions, the capped diglycolic acid would induce the aggregation of the NP probes upon encountering them; this was evidenced by the obvious red-shifting of the SPR peak and the enlarged size of the NPs. For the same reason, the selectivity of the probe for Cr(vi) against other heavy metal ions was found to be remarkable.

Exosomes derived from breast cancer lung metastasis subpopulations promote tumor self-seeding.

Lung metastasis is a primary obstacle in the clinical treatment of metastatic breast cancer. Most patients with lung metastasis eventually die of recurrence. Recurrence may be related to self-seeding, which occurs when circulating tumor cells re-seed into the tumors they originated from (metastasis or carcinoma in situ).

Preparation of elastic diglycolamic-acid modified chitosan sponges and their application to recycling of rare-earth from waste phosphor powder.

Inspired by the phenomenon of sponges soaking up water, a novel syringe-like adsorption device used diglycolamic-acid modified chitosan sponges (CSs-DGAA) as adsorbents is reported for recycling of rare-earth elements (REEs) by Squeezing & Soaking (S&S) operation. Integrating the elasticity of sponges and selective extraction ability of diglycolamic acid groups, the new device can efficiently recycle REEs from aqueous solutions. This device only needs 10 min to achieve adsorption equilibrium; squeezing the water from the sponges achieves solid-liquid separation.

Mitochondrial calcium uniporter as a target of microRNA-340 and promoter of metastasis via enhancing the Warburg effect.

Background: A shift from oxygen phosphorylation to aerobic glycolysis was known as the Warburg effect and a characteristic of cancer cell metabolism facilitating metastasis. Mitochondrial calcium uniporter (MCU), a key ion channel that mediates Ca uptake into mitochondria, was found to promote cancer progression and metastasis. However, its explicit role in shifting metabolism of breast cancer cells has not been defined.

STIM1 and STIM2 differently regulate endogenous Ca entry and promote TGF-β-induced EMT in breast cancer cells.

The Ca sensor proteins STIM1 and STIM2 are crucial elements of store-operated calcium entry (SOCE) in breast cancer cells. Increased SOCE activity may contribute to epithelial-mesenchymal transitions (EMT) and increase cell migration and invasion. However, the roles of STIM1 and STIM2 in TGF-β-induced EMT are still unclear.

Phosphorylation of dynamin-related protein 1 at Ser616 regulates mitochondrial fission and is involved in mitochondrial calcium uniporter-mediated neutrophil polarization and chemotaxis.

During an inflammatory response, polarization of neutrophils is necessary for effective chemotaxis and bacterial endocytosis. Ca uptake into mitochondria through the mitochondrial calcium uniporter (MCU) is crucial for cell metabolism, signaling and survival; however, the physiological role of MCU in human neutrophils remains unclear. Here we show that MCU is vital for the polarization and chemotaxis of neutrophils.

Downregulation of ACE2/Ang-(1-7)/Mas axis promotes breast cancer metastasis by enhancing store-operated calcium entry.

The renin-angiotensin system (RAS) is an important component of the tumor microenvironment and plays a key role in promoting cancer cell proliferation, angiogenesis, metabolism, migration and invasion. Meanwhile, the arm of angiotensin-converting enzyme (ACE)2/angiotensin-(1-7) [Ang-(1-7)]/Mas axis in connection with RAS is associated with anti-proliferative, vasodilatory and anti-metastatic properties. Previous studies have shown that Ang-(1-7) reduces the proliferation of orthotopic human breast tumor growth by inhibiting cancer-associated fibroblasts.

Store-operated Ca2+ entry plays a role in HMGB1-induced vascular endothelial cell hyperpermeability.

Aims: Endothelial dysfunction, including increased endothelial permeability, is considered an early marker for atherosclerosis. High-mobility group box 1 protein (HMGB1) and extracellular Ca2+ entry, primarily mediated through store-operated Ca2+ entry (SOCE), are known to be involved in increasing endothelial permeability. The aim of this study was to clarify how HMGB1 could lead to endothelia hyperpermeability.

Mitochondrial Ca²⁺ uniporter is critical for store-operated Ca²⁺ entry-dependent breast cancer cell migration.

Metastasis of cancer cells is a complicated multistep process requiring extensive and continuous cytosolic calcium modulation. Mitochondrial Ca(2+) uniporter (MCU), a regulator of mitochondrial Ca(2+) uptake, has been implicated in energy metabolism and various cellular signaling processes. However, whether MCU contributes to cancer cell migration has not been established.

[Polarization of neutrophils from patients with asthma, chronic obstructive pulmonary disease and asthma-chronic obstructive pulmonary disease overlap syndrome].

Objective: To explore the polarization of migration dynamics of neutrophils isolated from patients with asthma, chronic obstructive pulmonary disease (COPD) and asthma-COPD overlap syndrome (ACOS) compared with healthy smoking and non-smoking controls.

Methods: Recruited volunteers were classified as healthy controls, healthy smokers, asthma, COPD and ACOS at Nanfang Hospital from April 2013 to June 2014 according to the Global Strategy for the Diagnosis, Management and Prevention of COPD 2011, Global Strategy for Asthma Management and Prevention 2011 and Consensus on Overlap Phenotype COPD-asthma in COPD 2012. Neutrophils were freshly isolated from whole blood with density gradient technique.

Role of the mitochondrial Ca²⁺ uniporter in Pb²⁺-induced oxidative stress in human neuroblastoma cells.

Lead (Pb(2+)) has been shown to induce cellular oxidative stress, which is linked to changes in intracellular calcium (Ca(2+)) concentration. The mitochondrial Ca(2+) uniporter (MCU) participates in the maintenance of Ca(2+) homeostasis in neurons, but its role in Pb(2+)-induced oxidative stress is unclear. To address this question, oxidative stress was induced in human neuroblastoma SH-SY5Y cells and in newborn rats by Pb(2+) treatment.

Store-operated Ca²⁺ entry mediated regulation of polarization in differentiated human neutrophil-like HL-60 cells under hypoxia.

The regulation of neutrophil polarization by calcium entry is critical for maintaining an effective host response. Hypoxia has a major effect on the apoptosis of neutrophils, however the role of store-operated Ca2+ entry (SOCE) in neutrophil polarization under hypoxia remains to be elucidated. In the present study, we examined the polarization of differentiated human neutrophil-like HL-60 (dHL-60) cells exposed to hypoxia (3% O2) and the results demonstrated that the percentage of polarized cells following exposure to an N-formyl-Met-Leu-Phe (fMLP) gradient in the Zigmond chamber was increased.

TRPM7 mediates breast cancer cell migration and invasion through the MAPK pathway.

Metastasis is an inherent feature of breast cancer and transient receptor potential (TRP) channels were found to be potentially implicated in this process. Particularly, TRPM7 may regulate cell motility. We therefore examined the expression of TRPM7 mRNA in the Oncomine database and found that TRPM7 is correlated to metastasis and invasive breast cancer.

Requirement for both receptor-operated and store-operated calcium entry in N-formyl-methionine-leucine-phenylalanine-induced neutrophil polarization.

Tissue penetration of neutrophils is a key process in many inflammatory diseases. In response to inflammatory stimuli such as N-formyl-methionine-leucine-phenylalanine (fMLP), neutrophils polarize and migrate towards the chemotactic gradient of the stimulus. Elevated intracellular Ca(2+) concentration is known to play a critical role in neutrophil polarization and migration; however, the exact mechanism remains elusive.

Store-operated Ca2+ entry (SOCE) plays a role in the polarization of neutrophil-like HL-60 cells by regulating the activation of Akt, Src, and Rho family GTPases.

Neutrophil polarization is a basic activity involved in the innate immune response, and it may be initiated by extracellular Ca(2+) entry, a process primarily mediated through store-operated Ca(2+) entry (SOCE). Yet, the mechanisms by which SOCE participates in cell polarization remain unclear. We hypothesized that Akt- and Src-dependent pathways, traditionally linked to neutrophil polarization, may interact with SOCE in this event.

AKT-mediated regulation of polarization in differentiated human neutrophil-like HL-60 cells.

Objectives: Neutrophil polarization is critical for the inflammatory response. AKT is a serine/threonine protein kinase and has been implicated in cell migration. However, it is not completely clear whether AKT affects neutrophil polarization.

Effects of ZD7288 on firing pattern of thermosensitive neurons isolated from hypothalamus.

The role of the hyperpolarization-activated current (Ih) mediated by HCN channels in temperature sensing by the hypothalamus was addressed. In warm-sensitive neurons (WSNs), exposure to ZD7288, an inhibitor of Ih mediated by hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, decreased their action potential amplitudes and frequencies significantly. By contrast, ZD7288 had little or no effect on temperature-insensitive neurons (TINs).