GLS1 depletion inhibited colorectal cancer proliferation and migration via redox/Nrf2/autophagy-dependent pathway.

Cancer cells can metabolize glutamine to replenish TCA cycle intermediates for cell survival. Glutaminase (GLS1) is over-expressed in multiple cancers, including colorectal cancer (CRC). However, the role of GLS1 in colorectal cancer development has not yet fully elucidated. In this study, we found that GLS1 levels were significantly increased in CRC cells. Knockdown of GLS1 by shRNAs as well as GLS1 inhibitor BPTES decreased DLD1 and SW480 cell proliferation, colony formation and migration. Knockdown of GLS1 as well as BPTES induced reactive oxygen species (ROS) production, down-regulation of GSH/GSSG ratio, an decrease in Nrf2 protein expression and an increase in cytoplasmic Nrf2 protein expression in DLD1 and SW480 cells. Furthermore, Knockdown of GLS1 as well as BPTES inhibited autophagy pathway, antioxidant NAC and Nrf2 activator could reversed inhibition of GLS1-mediated an decrease in autophagic flux in DLD1 and SW480 cells. Depletion of GLS1-induced inhibition of DLD1 and SW480 CRC cell proliferation, colony formation and migration was reversed by autophagy inducer rapamycin. These results suggest that targeting GLS1 might be a new potential therapeutic target for the treatment of CRC.

FOXM1 facilitates breast cancer cell stemness and migration in YAP1-dependent manner.

Breast cancer has the highest incidence and mortality in the female population. Forkhead box M1 (FOXM1) known as a transcription factor is upregulated and associated with poor prognosis in a variety of cancers. However, the molecular mechanisms of FOXM1 on breast cancer progression are poorly understood. In this study, we found that FOXM1 was up-regulated in breast cancer. FOXM1 promoted cell proliferation, clonal formation, and migration capacity in triple negative breast cancer by increasing transcriptional activity of YAP1. FOXM1 also maintained cell stemness via the Hippo pathway. The YAP1-TEAD binding inhibitor Verteporfin reduced the transcription level of OCT4 and NANOG but the Hippo pathway activator XMU-MP-1 could increase the transcription level of OCT4 and NANOG. In summary, our findings indicated that FOXM1 promoted breast cancer progression through the Hippo pathway, and it was suggested a new strategy to treat breast cancer.

KDM5B promotes breast cancer cell proliferation and migration via AMPK-mediated lipid metabolism reprogramming.

Lysine demethylase 5B (KDM5B) is up-regulated in many cancers, including breast cancer. However, the underlying metabolic mechanisms of KDM5B on breast cancer progression are poorly understood. Here, we showed that KDM5B expression positively correlates with metastasis in breast cancer. Cell functional analyses were demonstrated that KDM5B knockdown and KDM5B inhibitor AS-8351 inhibited breast cancer cell proliferation and migration. Furthermore, we reported that KDM5B knockdown and AS-8351 reversed epithelial-mesenchymal transition (EMT) and decreased the protein levels of fatty acid synthase (FASN) and ATP citrate lyase (ACLY) in MCF-7 and MDA-MB-231 cells. Interestingly, we found that activation of AMP-activated protein kinase (AMPK) signaling pathway is involved in KDM5B-mediated EMT and lipid metabolism reprogramming in breast cancer cells. As a result, silencing of KDM5B-induced activation of AMPK signaling pathway inhibited breast cancer cell proliferation and migration. Taken together, our findings indicated that KDM5B was a novel regulator of lipid metabolism reprogramming, and it was suggested a new strategy to treat breast cancer.

A remaining useful life estimation method based on long short-term memory and federated learning for electric vehicles in smart cities.

In modern society, environmental sustainability is a top priority as one of the most promising entities in the new energy sector. Electric vehicles (EVs) are rapidly gaining popularity due to their promise of better performance and comfort. Above all, they can help address the problem of urban air pollution. Nonetheless, lithium batteries, one of the most essential and expensive components of EVs, have posed challenges, such as battery aging, personal safety, and recycling. Precisely estimating the remaining useful life (RUL) of lithium battery packs can effectively assist in enhancing the personal safety of EVs and facilitating secondary trading and recycling in other industries without compromising safety and reliability. However, the RUL estimation of batteries involves many variables, and the operating conditions of EV batteries are highly dynamic as they change with the environment and the driving style of the users. Many existing methods exist to estimate the RUL based on batteries' state of health (SOH), but only some are suitable for real-world data. There are several difficulties as follows. Firstly, obtaining data about battery usage in the real world takes work. Secondly, most of these estimation models must be more representative and generalized because they are trained on separate data for each battery. Lastly, collecting data for centralized training may lead to a breach of user privacy. In this article, we propose an RUL estimation method utilizing a deep learning (DL) approach based on long short-term memory (LSTM) and federated learning (FL) to predict the RUL of lithium batteries. We refrain from incorporating unmeasurable variables as inputs and instead develop an estimation model leveraging LSTM, capitalizing on its ability to predict time series data. In addition, we apply the FL framework to train the model to protect users' battery data privacy. We verified the results of the model on experimental data. Meanwhile, we analyzed the model on actual data by comparing its mean absolute and relative errors. The comparison of the training and prediction results of the three sets of experiments shows that the federated training method achieves higher accuracy in predicting battery RUL compared to the centralized training method and another DL method, with solid training stability.

Highly efficient and selective adsorption of heavy metal ions by hydrazide-modified sodium alginate.

In the present study, a new potential adsorbent for the separation and removal of heavy metal ions was prepared using hydrazide modification. Characterization of structural and chemical properties of the absorbent indicated the dialdehyde sodium alginate (DSA) grafted adipic acid dihydrazide (AAD) plays a crucial role. The adsorption process correlated well with Freundlich isotherm and pseudo-second-order kinetics models. Additionally, the adsorption capacities for Hg2+, Pb2+, Cd2+, and Cu2+ were 7.833, 2.036, 4.766, and 3.937 mmol g-1, respectively. The thermodynamic parameter for the sorption demonstrated the process is endothermic and spontaneous. FT-IR and XPS analysis revealed the combination of chelation interactions and ion exchange between nitrogen, oxygen atoms and heavy metal ions. Moreover, after 10 times adsorption-desorption recycles, the adsorption efficiency of the adsorbent was slightly decreased. In conclusion, the as-prepared adsorbent has great potential in practical water pollution purification.

Effective removal of metal ions and cationic dyes from aqueous solution using different hydrazine-dopamine modified sodium alginate.

In this paper, DSA-AAD-DA and DSA-TPDH-DA were prepared to effectively remove metal ions and cationic dyes from aqueous solution. The hydrazone structure was prepared by hydrazide-modified SA which captured metal ions selectively, and the remaining functional groups were used as active adsorption sites for cationic dyes. The thermodynamic parameter for the sorption demonstrated the process is endothermic and spontaneous. In single process, the adsorption of metal ions by DSA-AAD-DA and DSA-TPDH-DA correlated well with the Freundlich model through the hydrazone structure coordination and ion exchange which was mainly chemical adsorption, and cationic dyes adsorption correlated well with the Langmuir model which was shown monolayer adsorption was dominant by hydrogen bonding, electrostatic interaction, and π-π interaction. In binary system, the mixed adsorption shown significant antagonism effect in high concentration, but cationic dyes and metal ions in low concentration were efficiently and simultaneously removed, the adsorption ability of DSA-TPDH-DA was much better than DSA-AAD-DA. Moreover, adsorption efficiency can still maintain more than 80% after five times adsorption-desorption recycle. Therefore, DSA-AAD-DA and DSA-TPDH-DA possessed great potential for wastewater treatment.

A rhodamine derivative probe for highly selective detection of Cu(II).

BACKGROUND: Abnormal Cu(II) ions levels may affect many biological functions, and it is of great importance to detect Cu(II) ions in organisms. METHODS: Herein, we report a near-infrared (NIR) fluorescent probe EtRh-N-NH2 for the detection of Cu(II). In the probe structure, a rhodamine core was used, and a hydrazine group was employed as the responsive site. Results & Conlusions: EtRh-N-NH2 displayed sensitive, specific and fast response upon Cu(II) with excellent linear relationship between the concentration and fluorescence emission intensity in 0-1 µM range. The releasing EtRh-COOH exhibited 762 nm of emission wavelength with a 75 nm of Stokes shift.

TIGAR drives colorectal cancer ferroptosis resistance through ROS/AMPK/SCD1 pathway.

Colorectal cancer (CRC) is the third most commonly diagnosed malignancy and major cause of cancer death in the world. Ferroptosis is a recently identified type of regulated cell death. Increasing evidence has shown that ferroptosis plays an important regulatory role in the occurrence and development of cancer. This study identified TIGAR as a potential regulator of ferroptosis resistance in the development of CRC. We showed that TIGAR expression in CRC tissues is significantly higher than that in adjacent normal tissues. Knockdown of TIGAR significantly caused an increase in erastin-induced ferroptosis in SW620 and HCT116 cells. Notably, knockdown of TIGAR significantly decreased GSH/GSSG ratio, increased lipid peroxidation production, and facilitated the accumulation of lipid peroxidation product malondialdehyde (MDA), and rendered CRC cells more sensitive to erastin induced ferroptosis. Furthermore, TIGAR inhibition repressed SCD1 expression in a redox and AMPK-dependent manner. Thus, these results suggest that TIGAR induces ferroptosis resistance in CRC cells via the ROS/AMPK/SCD1 signaling pathway.

Magnetic cross-linked chitosan for efficient removing anionic and cationic dyes from aqueous solution.

Herein, a novel magnetic cross-linked chitosan CS-BA@Fe3O4 was rationally synthesized by cross-linked with epichlorohydrin and coated with Fe3O4 to the acylated chitosan, which was prepared by the reaction of chitosan with benzenetricarboxylic anhydride. The as-obtained absorbent was characterized by FTIR, XRD, VSM, TGA, TEM, BET, SEM and EDS. The results showed that the maximum adsorption capacities of CR and CV were 471.46 ± 16.97 mg/g and 515.91 ± 25.12 mg/g at 318.15 K, respectively. The main adsorption mechanisms were H-bonding and electrostatic interaction. The kinetic data were in good agreement with the pseudo-second-order model and closed to adsorption equilibrium at 30 min. Thermodynamic studies showed that the adsorption on CS-BA@Fe3O4 were spontaneous and endothermic. More importantly, the adsorbent exhibited excellent regeneration properties after 6 cycles and remarkable stability under harsh environments including strong acid, strong alkali, multi-salt and mixed dyes conditions. Therefore, abundant efforts revealed a broad application prospect of CS-BA@Fe3O4 in water remediation.

TSPAN8 promotes colorectal cancer cell growth and migration in LSD1-dependent manner.

AIMS: Colorectal cancer (CRC) is the fourth leading cause of cancer-related mortality worldwide. Over-expression of tetraspanin 8 (TSPAN8) is related to the development and progression of CRC. Whether TSPAN8 plays a role in the growth of colorectal cancer and its epigenetic mechanisms regulated by Lysine Specific Demethylase 1 (LSD1) are still unknown. MAIN METHODS: In this study, RT-PCR and western blotting were used to analyze the mRNA and protein expression, respectively; cell viability was assayed with MTS analysis; cell migration was measured with Trans-well analysis. KEY FINDINGS: In the present study, the results indicated that the mRNA levels of LSD1 and TSPAN8 in CRC were significantly higher than that in corresponding adjacent non-tumor tissue. Down-regulation of LSD1 or TSPAN8 as well as LSD1 inhibitor Tranylcypromine hemisulfate inhibited the proliferation and migration of CRC cells, while over-expression of LSD1 exhibited opposite effects. LSD1 up-regulated TSPAN8 expression and reduced H3K9me2 occupancy on the TSPAN8 promoter in CRC cells. TSPAN8 promoted epithelial-mesenchymal transition (EMT) in CRC cells in LSD1-dependent manner. SIGNIFICANCE: TSPAN8 may be considered as a promising biomarker for the diagnosis and prognosis in patients with CRC. Furthermore, TSPAN8 could be a novel therapeutic target and potent LSD1 inhibitors could be designed and developed in the treatment of CRC.

Purification of recombinant laccase from Trametes versicolor in Pichia methanolica and its use for the decolorization of anthraquinone dye.

A recombinant laccase from Trametes versicolor in Pichia methanolica was produced constitutively in a defined medium. The recombinant laccase was purified using ultrafiltration, anion-exchange chromatography, and gel filtration. The molecular weight of the purified laccase was estimated as 64 kDa by SDS-PAGE. The purified recombinant laccase decolorized more than 90% of Remazol Brilliant Blue R (RBBR) initially at 80 mg l(-1) after 16 h at 45 degrees C and pH 5 when 25 U laccase ml(-1) was used. The purified recombinant laccase could efficiently decolorize RBBR without additional redox mediators.