Ying-Yu Ma

Brain tumors, particularly gliomas, are among the most lethal malignancies, with high mortality driven by a delayed diagnosis and limited therapeutic efficacy. A central challenge lies in the presence of the blood‑brain barrier (BBB), which severely impedes the delivery of systemically administered therapeutics to tumor sites. Addressing this clinical urgency, nanoparticle (NP)‑based delivery systems have emerged as a transformative strategy to enhance brain‑specific drug accumulation, minimize off‑target toxicity and improve treatment outcomes. The present review systematically examined the recent advances in nanocarrier technologies for targeted brain tumor therapy, including liposomes, solid lipid NPs, dendrimers, polymeric nanoplatforms and inorganic nanomaterials. The design principles, mechanisms for BBB traversal, therapeutic payload compatibility and tumor‑targeting capabilities of NP technologies demonstrated in preclinical models have also been highlighted. In addition to drug delivery, emerging applications of nanocarriers in gene therapy were explored and the impact of protein corona formation on NP behavior in vivo was discussed. Finally, current translational bottlenecks were identified and future design considerations to achieve clinically viable, precision‑targeted nanomedicines for brain tumors were outlined.

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease worldwide. With the rising prevalence of diabetes, the occurrence of DN is likely to hit pandemic proportions. The current treatment strategies employed for DN focus on the management of blood pressure, glycemia, and cholesterol while neglecting DN’s molecular progression mechanism. For many theranostic uses, nano-technological techniques have evolved in biomedical studies. Several nanotechnologically based theranostics have been devised that can be tagged with targeting moieties for both drug administration and/or imaging systems and are being studied to identify various clinical conditions. The molecular mechanisms involved in DN are discussed in this review to assist in understanding its onset and progression pattern. We have also discussed emerging strategies for establishing a nanomedicine-based platform for DN-targeted drug delivery to increase drug’s efficacy and safety, as well as their reported applications.

PHF21A expression as a biomarker of hepatocellular carcinoma progression and prognosis

Purpose: SLC41A3 is a member of the solute carrier family 41 (SLC41) and is involved in many cellular processes as a magnesium ion transporter. Although it plays an important role in cancer formation and development, the correlation between the expression of SLC41A3 and the occurrence and prognosis of hepatocellular carcinoma (HCC) remains unclear. Therefore, this study was focused on the evaluation of the relationship between SLC41A3 and the development and prognosis of HCC. Patients and Methods: Firstly, we collected the mRNA expression of SLC41A3 in HCC through the platform of Oncomine. Then, the subgroups of HCC were performed by the UALCAN website and the prognosis of HCC was analyzed by Kaplan–Meier Plotter database. Subsequently, immunohistochemistry (IHC) method was used to detect SLC41A3 expression in 323 clinically confirmed HCC samples and 184 non-cancerous liver tissues. Finally, function enrichment analysis was done using the LinkInterpreter module in LinkedOmics, and gene set enrichment analysis (GSEA) was performed using TCGA data set. Results: The Oncomine database and immunohistochemical (IHC) showed higher SLC41A3 expression in HCC tissue compared to normal tissue. The expression of SLC41A3 was significantly correlated with tumor metastasis, Edmondson grade, microvascular invasion, and AFP level. Kaplan–Meier and Cox regression analyses verified that high SLC41A3 expression is a significant prognostic factor for reduced overall survival in HCC patients. Conclusion: Our results demonstrated that high expression of SLC41A3 was the predictor of poor prognosis in HCC patients, suggesting that this protein may be a potential target for HCC therapy.

Resveratrol alleviates intestinal mucosal barrier dysfunction in dextran sulfate sodium-induced colitis mice by enhancing autophagy

Numerous epidemiological studies have evaluated the association between the CDH1 -160C/A polymorphism and the risk of breast cancers. However, these studies have yielded conflicting results. To derive a more precise estimation of this association, this meta-analysis was conducted. A comprehensive search using the keywords “CDH1,” “E-Cadherin,” “polymorphism,” “SNP,” and “variant” combined with “breast,” “cancer,” “tumor,” or “carcinomas” was conducted. Pooled odds ratios (ORs) with 95 % confidence intervals (CIs) were appropriately calculated using a fixed effect or random effect model. Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2009 checklist was used for this meta-analysis. Four publications including five studies were identified. It was found that the CDH1 -160C/A polymorphism was significantly associated with breast cancer risk in the dominant model (CA + AA vs. CC: OR = 1.207, 95 % CI = 1.031–1.412, P = 0.019). Our meta-analysis demonstrated that the -160C/A polymorphism in the CDH1 gene might contribute to breast cancer susceptibility. Further investigations using a much larger sample including different ethnicities are still needed to verify this association.

In chronic obstructive pulmonary disease (COPD), two major pathological changes that occur are the loss of alveolar structure and airspace enlargement. To treat COPD, it is crucial to repair damaged lung tissue and regenerate the lost alveoli. Type II alveolar epithelial cells (AECII) play a vital role in maintaining lung tissue repair, and amniotic fluid-derived mesenchymal stromal cells (AFMSCs) possess the characteristics of regular mesenchymal stromal cells. However, it remains untested whether transplantation of rat AFMSCs (rAFMSCs) might alleviate lung injury caused by emphysema by increasing the expression of surfactant protein (SP)A and SPC and inhibiting AECII apoptosis. We analyzed the phenotypic characteristics, differentiation potential, and karyotype of rAFMSCs, which were isolated from pregnant Sprague–Dawley rats. Moreover, we examined the lung morphology and the expression levels of SPA and SPC in rats with emphysema after cigarette-smoke exposure and intratracheal lipopolysaccharide instillation and rAFMSC transplantation. The ability of rAFMSCs to differentiate was measured, and the apoptosis of AECII was evaluated. In rAFMSCs, the surface antigens CD29, CD44, CD73, CD90, CD105, and CD166 were expressed, but CD14, CD19, CD34, and CD45 were not detected; rAFMSCs also strongly expressed the mRNA of octamer-binding transcription factor 4, and the cells could be induced to differentiate into adipocytes and osteocytes. Furthermore, rAFMSC treatment up-regulated the levels of SPA, SPC, and thyroid transcription factor 1 and inhibited AECII apoptosis, and rAFMSCs appeared to be capable of differentiating into AECII-like cells. Lung injury caused by emphysema was alleviated after rAFMSC treatment. rAFMSCs might differentiate into AECII-like cells or induce local regeneration of the lung alveolar epithelium in vivo after transplantation and thus could be used in COPD treatment and lung regenerative therapy.

Background: Recent studies have shown that miR-199a-5p plays opposite roles in cancer initiation and progression of different cancer types, acting as oncogene for some cancer types but as tumor suppressor gene for others. However, the role and molecular mechanism of miR-199a-5p in gastric cancer are largely unknown. Methods: In this study, miR-199a-5p expression level in gastric cancer was first analyzed by qPCRand then validated in 103 gastric cancer patients by in situ hybridization (ISH). Gastric cancer cell lines were transfected with miR-199a-5p inhibitor and mimic, and underwent in vitro transwell assays. Target genes (klotho) were identified using Luciferase reporter assay. Immunohistochemical staining was also used to investigate on how miR-199a-5p regulates the tumour-suppressive effects of klotho in gastric cancer. Results: In our present study, we found that miR-199a-5p level was significantly increased in gastric cancer tissues compared to paired normal tissues. We observed that miR-199a-5p could promote migration and invasion of gastric cancer cells. In situ hybridization of miR-199a-5p also confirmed that higher miR-199a-5p expression level was associated with increased likelihood of lymph node metastasis and later TNM stage. Luciferase reporter assay and immunohistochemistry revealed that klotho might be the downstream target of miR-199a-5p. Conclusions: Our present study suggests that miR-199a-5p acts as an oncogene in gastric cancer and functions by targeting klotho.

Background: Golgi protein 73 (GP73) is a type II Golgi transmembrane protein. It is over-expressed in several cancers, including hepatocellular carcinomas, bile duct carcinomas, lung cancer and prostate cancer. However, there are few reports of GP73 in gastric cancer. This study is aimed at investigating the expression of GP73 and its relationship with clinical pathological characters in gastric cancer. Methods: GP73 mRNA level was determined by quantitative real-time RT-PCR in 41 pairs of matched gastric tumorous tissues and adjacent non-tumorous mucosal tissues. Western blotting was also performed to detect the GP73 protein level. GP73 protein expression was analyzed by immunohistochemistry in 52 clinically characterized gastric cancer patients and 10 non-tumorous gastric mucosal tissue controls. Results: The mRNA and protein level of GP73 were significantly down-regulated in gastric tumorous tissues compared with the non-tumorous mucosal tissues. In non-tumorous mucosa, strong diffuse cytoplasmic staining can be seen in cells located at the surface of the glandular and foveolar compartment; while in tumorous tissues, the staining was much weaker or even absent, and mainly in a semi-granular dot-like staining pattern. The expression level of GP73 protein was associated with patients’ gender and tumor differentiation. Conclusions: GP73 was normally expressed in non-tumorous gastric mucosa and down-regulated in gastric cancer. Its expression in gastric cancer was correlated with tumor differentiation.