Open Life Sciences最新文献

Pectin has bad effects on the sensory quality of cigarettes. In order to reduce the pectin content in tobacco leaves, polygalacturonase (PG) gene was extracted from Aspergillus niger sw06, and recombinant plasmid pPICZαA was constructed and transformed into Pichia pastoris X33 to build an engineered strain X33/pPICZαA-PG. Transformant genomic fragment was 1,608 bp. The genomic fragment was amplified and recovered, and sequencing indicated that PG gene expression have been successfully inserted into P. pastoris expression vector. Positive clones were detected by SDS protein with a molecular weight of about 60 kDa. The enzyme production cycle of the recombinant strain was 36 h, and crude enzyme activity was 2872.91 U/mL. The fusion protein was purified by nickel Sepharose affinity chromatography. A clear band was detected and the concentration of recombinant protein was 8.1 μg/μL. It showed a good effect on degrading pectin after addition of the PG crude enzyme produced by recombinant yeast on the tobacco pulp. The optimized addition amount on process product line was 0.8%, which could reduce tobacco pulp pectin from 3.65 to 3.01% and achieve a degradation rate of 17.53%. Sensory evaluation showed that the effect was better when the addition amount of pulping was 0.4%.

Lung cancer is one of the most common and deadly malignancies worldwide, underscoring the need for reliable biomarkers that can inform prognosis and guide postoperative surveillance. This prospective study examined longitudinal changes in 10 tumor-associated autoantibodies in 71 patients with early-stage non-small-cell lung cancer (NSCLC) who underwent surgical resection. Blood samples were collected preoperatively and at 3-, 6-, and 12-month post-surgery. Enzyme-linked immunosorbent assays were used to measure serum autoantibodies against p53, MUC1, NY-ESO-1, APE1, PGP9.5, SOX2, GBU4-5, GAGE7, CAGE, and MAGE1. Logistic regression models assessed associations with 1-year recurrence, while Cox proportional hazards models evaluated overall survival. Substantial reductions in p53, GBU4-5, and CAGE autoantibodies correlated with lower recurrence risk and improved 1-year survival, even after false discovery rate adjustment (p < 0.05). NY-ESO-1 showed borderline significance for recurrence, and SOX2 was borderline for survival but did not remain significant after correction. These findings suggest that monitoring dynamic declines in certain autoantibodies (most notably CAGE) may offer clinically meaningful prognostic information following surgical resection. While further validation in larger, independent cohorts is required, our results highlight the potential of serial autoantibody profiling as a noninvasive tool for personalized postoperative management in early-stage NSCLC patients.

Cancer treatment continues to face challenges due to adverse effects, drug resistance linked with conventional therapies, and high costs. As increasing interest in safer and cost-effective alternatives drugs, natural products such as flavonoids have been explored for treating cancer. Rutin, a dietary flavonoid, exhibits diverse pharmacological activities that may contribute to cancer prevention and treatment. It interferes with cancer progression by inducing apoptosis and autophagy, promoting cell cycle arrest, regulating oxidative stress, activating tumor suppressor gene, and modulating various signaling cascades. Recent studies also suggest that combining rutin with other therapeutic agents or employing nanoformulations may enhance its bioavailability and anticancer efficacy. This review critically examines anticancer mechanisms across various cancer types and highlights novel strategies to explored their therapeutic potential. The comprehensive clinical trials and mechanistic studies are needed to validate its safety, bioavailability, and efficacy in cancer management.

To investigate the effect of coal industry-related airborne particulate matter (PM) on ocular surface tear film injury and inflammatory factor expression. Male Sprague-Dawley (SD) rats were randomly divided into the treatment group and the normal control group, with five rats in each group. A dust chamber was used to simulate the air contamination conditions associated with the coal industry. Tear secretion, tear-film breakup time (BUT), conjunctival congestion score, and relative expression levels of tear inflammatory factors, including interleukin (IL)-6, IL-17, and tumor necrosis factor (TNF)-α, were compared between the treatment group and the normal control group. After 4 weeks' exposure, tear secretion (2.64 ± 0.57 mm vs 5.42 ± 0.28 mm), BUT (4.23 ± 0.47 s vs 6.15 ± 0.36 s), and conjunctival congestion score [2 (2, 3) vs 0 (0, 1)] were significantly different between the treatment group and the control group (all P < 0.05), and hematoxylin-eosin stain showed that the number of goblet cells decreased in the treatment group. In addition, the relative expression levels of IL-6, IL-17, and TNF-α in tears of the treatment group were significantly different from those of the normal control group (all P < 0.05). Coal industry-related airborne PM exposure can damage tear film function and increase relative expression levels of tear inflammatory factors in SD rats.

Lanthanum (La) accumulates resulted in detrimental alterations in the morphology and structure of hippocampal neurons, but the specific mechanism remains unclear. At 49 days after the birth of LaCl₃-exposed offspring rats, number of Nissl bodies and the neural cell structure in hippocampal tissue was evaluated by Nissl and HE staining; the ultrastructure of hippocampal CA1 zone was observed by electron microscopy. Learning and memory ability of the offspring decreased after LaCl₃ exposure. Nissl staining showed that in the La-exposed rats, Nissl body number in the hippocampus was significantly decreased, and the cell arrangement was disordered. The ultramicroscopic structure of hippocampal neurons in La-exposed rats showed that the mitochondrial volume was increased; ridges were shorter, decreased in number, and marginally shifted; and the matrix electron density was also decreased. The contents of TNFR1, P-RIPK1, P-RIPK3, and P-MLKL in hippocampal neurons increased significantly as the LaCl₃ dose increased. La exposure retarded the growth and development of offspring rat, resulted hippocampal nerve cell necroptosis, and impaired spatial learning and memory, which related to abnormal expression of TNFR-RIPK1/RIPK3 pathway.

The large demand for Roman chamomile essential oil leads to nonnegligible residues in the process of steam distillation. It is an urgent problem to recycle these residues to solve the pollution in the ecological environment and enhance the industrial value. In this study, the components of different fractions extracted from the Roman chamomile residue were analyzed, and their antioxidant, whitening, and anti-aging activities were evaluated. It was found that the crude extract (CE) contained large amounts of polyphenols and flavonoids and displayed obvious antioxidant, whitening, anti-aging activities, and extremely low cytotoxicity. After fractional extraction, polyphenols and flavonoids were largely enriched in the ethyl acetate fraction (EaF), and total polyphenols and total flavonoids increased three- and fourfold, respectively, compared with CE. Especially, the rutin content increased 5.18-fold, quercetin increased 7.29-fold, and luteolin increased 10.58-fold. While chlorogenic acid and p-coumaric acid were mainly enriched in n-butanol fraction (NbF), and increased 2.1- and 2.75-fold than that in CE, respectively. The antioxidant, whitening and anti-aging activities of EaF are significantly higher than those of CE, especially the inhibition for hyaluronidase, elastase were greater than those of epigallocatechin gallate (EGCG), and its inhibitory effects on the tyrosinase and melanin content in B16F10 cells were stronger than those of kojic acid. NbF also showed lower IC₅₀ values than EGCG against hyaluronidase and elastase. These results indicated that the Roman chamomile residue, especially the CE, EaF, and NbF, had excellent antioxidant, whitening, and anti-aging activities and could be a new natural raw material for use in functional cosmetic formulations.

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide, and emerging evidence implicates circadian rhythm disruption in its pathogenesis. Here, we identified the core circadian gene Cryptochrome1 (Cry1) as a potential tumor suppressor in HCC. Clinical analysis revealed that low Cry1 expression correlated with poor prognosis, showing a median survival of 36 vs 47 months, and Cry1 expression was significantly reduced in HCC cell lines (0.6-fold in SMMC-7721 vs LO2). Functional studies demonstrated that Cry1 overexpression reduced proliferation by 30% with more cells in the G1 phase, as well as inhibited migration/invasion, while Cry1 knockdown increased proliferation by 50% with less cells in the G1 phase and increased migration/invasion. Finally, we found Cry1 depletion downregulated pro-apoptotic BAX and upregulated anti-apoptotic BCL2, while Cry1 overexpression produced the opposite effects, suggesting its role in apoptosis via the BCL2/BAX-mediated apoptosis pathway. These findings indicate that Cry1 acts as a tumor suppressor in HCC, providing insights into the circadian dysfunction-cancer pathogenesis connection and its potential as a diagnostic biomarker and therapeutic target requires further verification through preclinical and clinical investigations in the future.

Renal cell carcinoma (RCC) is an aggressive malignancy with a poor prognosis influenced by pyroptosis in tumor-associated M2 macrophages. This study investigated how kynurenine modulates pyroptosis in M2 macrophages and promotes RCC progression. M2 macrophages were treated with pyroptosis inhibitor VX-765 or kynurenine to evaluate their effects on cell viability and pyroptosis. Transwell co-culture systems were employed to assess the impact of M2 macrophages on RCC cell proliferation, colony formation, and viability. The interaction between kynurenine and CASP1 (caspase-1), a key executor of pyroptosis that cleaves gasdermin D (GSDMD) to trigger inflammatory cell death, was analyzed using surface plasmon resonance. The results demonstrated that VX-765 treatment significantly enhanced M2 macrophage viability while reducing pyroptosis, thereby promoting RCC cell proliferation in co-culture systems. Kynurenine significantly enhanced M2 macrophage viability while suppressing pyroptosis. Mechanistically, kynurenine reduced the cleavage of CASP1 (caspase-1) by directly binding to it. Overexpression of CASP1 reversed kynurenine-induced suppression of pyroptosis in M2 macrophages. Furthermore, CASP1 overexpression abolished kynurenine-mediated enhancement of RCC cell viability, colony formation, and proliferation. This study revealed that kynurenine inhibits pyroptosis in M2 macrophages via direct targeting of CASP1, creating a tumor-supportive microenvironment that accelerates RCC progression. These findings establish the kynurenine-CASP1 axis as a critical regulator of M2 macrophage pyroptosis and demonstrate its role in promoting RCC progression, identifying a potential therapeutic target for RCC treatment.

Radiotherapy is an important cancer treatment for breast cancer patients, improving overall survival; however, it can lead to a common complication, radiation-induced heart disease (RIHD). N6-methyladenosine (m6A) RNA modification plays a critical role in the regulation of myocardial function. The aim of this study is to investigate the effect of m6A modification on cardiac injury following radiotherapy for breast cancer. Cardiac dysfunction was assessed by echocardiography and hematoxylin and eosin staining. The expression of ALKBH5 was analyzed by quantitative real-time PCR, western blot, and immunohistochemistry. The underlying mechanism was investigated using methylated RNA immunoprecipitation (MeRIP), RIP, and dual-luciferase reporter assays. The results showed that in RIHD, ALKBH5 expression was upregulated in breast cancer patients after radiotherapy and in RIHD mouse models. ALKBH5 downregulated the m6A modification level of Toll-like receptor 4 (TLR4). Overexpression of TLR4 abolished the inhibitory effect of ALKBH5 silencing on RIHD in mice. In summary, this study revealed a novel regulatory mechanism of ALKBH5-mediated m6A demethylation in RIHD, which could provide a promising therapeutic strategy for cardiac dysfunction following radiotherapy in breast cancer patients.

Gastric cancer is among the most common gastrointestinal malignancies with high morbidity and mortality rates, highlighting the need to further elucidate its pathogenesis and identify effective therapeutic targets. The regulatory factor X (RFX) gene family encodes transcription factors implicated in the development and progression of several cancers. Although RFX5 has been reported to influence tumor progression in various malignancies, its specific role in gastric adenocarcinoma remains unclear. In this study, we investigated the functional effects of RFX5 in gastric adenocarcinoma. Our findings revealed that RFX5 is highly expressed in gastric adenocarcinoma tissues. Silencing of RFX5 significantly inhibited cell proliferation and migration, while promoting apoptosis in gastric adenocarcinoma cells. Mechanistically, RFX5 knockdown activated the silent information regulator transcript 1/adenosine monophosphate-activated protein kinase (SIRT1/AMPK) signaling axis. These results suggest that RFX5 facilitates the growth and motility of gastric adenocarcinoma cells and suppresses apoptosis, at least in part, through modulation of the SIRT1/AMPK pathway.