Role of autophagy-related genes in liver cancer prognosis.

Autophagy, a highly conserved process of protein and organelle degradation, has emerged as a critical regulator in various diseases, including cancer progression. In the context of liver cancer, the predictive value of autophagy-related genes remains ambiguous. Leveraging chip datasets from the TCGA and GTEx databases, we identified 23 differentially expressed autophagy-related genes in liver cancer. Notably, five key autophagy genes, PRKAA2, BIRC5, MAPT, IGF1, and SPNS1, were highlighted as potential prognostic markers, with MAPT showing significant overexpression in clinical samples. In vitro cellular assays further demonstrated that MAPT promotes liver cancer cell proliferation, migration, and invasion by inhibiting autophagy and suppressing apoptosis. Subsequent in vivo studies further corroborated the pro-tumorigenic role of MAPT by suppressing autophagy. Collectively, our model based on the five key genes provides a promising tool for predicting liver cancer prognosis, with MAPT emerging as a pivotal factor in tumor progression through autophagy modulation.

Regorafenib-induced renal-limited thrombotic microangiopathy: a case report and review of literatures.

BACKGROUND: Regorafenib belongs to a sub-group of small-molecule multi-targeted tyrosine kinase inhibitors(TKIs). In various studies with respect to the side-effect of regorafenib, drug-associated proteinuria standardly qualified to be defined as nephrotic syndrome was rarely reported as well as the relation of regorafenib with the occurrence and development of thrombotic microangiopathy (TMA). CASE PRESENTATION: In this case report and literature review, we presented a 62-year-old patient receiving regorafenib for metastatic colon cancer, manifesting abundant proteinuria, in which TMA was also diagnosed through renal biopsy. As far as we were concerned, this was the first reported in terms of regorafenib-induced TMA confirmed by renal biopsy. CONCLUSION: This case indicates that regorafenib, a kind of TKIs may result in TMA, which is a rare but life-threatening complication of cancer treatment drug. Insights from this case might help physicians diagnose rare forms of TMA and adjust treatment for patients in a timely manner.

Atypical anti-glomerular basement membrane disease with anti-GBM antibody negativity and ANCA positivity: a case report.

BACKGROUND: Anti-glomerular basement membrane (anti-GBM) disease is an organ-specific autoimmune disease that involves the lung and kidneys and leads to rapid glomerulonephritis progression, with or without diffuse alveolar hemorrhage, and even respiratory failure. Classic cases of anti-GBM disease are diagnosed based on the presence of the anti-GBM antibody in serum samples and kidney or lung biopsy tissue samples. However, atypical cases of anti-GBM disease are also seen in clinical practice. CASE PRESENTATION: We herein report the rare case of a patient with atypical anti-GBM disease whose serum was negative for the anti-GBM antibody but positive for the myeloperoxidase (MPO) anti-neutrophil cytoplasmic antibody (p-ANCA) and another atypical ANCA. Laboratory test results showed severe renal insufficiency with a creatinine level of 385 µmol/L. Renal biopsy specimen analysis revealed 100% glomeruli with crescents; immunofluorescence showed immunoglobulin G (IgG) linearly deposited alongside the GBM. Finally, the patient was discharged successfully after treatment with plasmapheresis, methylprednisolone and prednisone. CONCLUSION: This patient, whose serum was negative for the anti-GBM antibody but positive for p-ANCA and another atypical ANCA, had a rare case of anti-GBM disease. Insights from this unusual case might help physicians diagnose rare forms of glomerulonephritis and treat affected patients in a timely manner.

Exendin-4 Ameliorates Lipotoxicity-induced Glomerular Endothelial Cell Injury by Improving ABC Transporter A1-mediated Cholesterol Efflux in Diabetic apoE Knockout Mice.

ATP-binding cassette transporter A1 (ABCA1), which promotes cholesterol efflux from cells and inhibits inflammatory responses, is highly expressed in the kidney. Research has shown that exendin-4, a glucagon-like peptide-1 receptor (GLP-1R) agonist, promotes ABCA1 expression in multiple tissues and organs; however, the mechanisms underlying exendin-4 induction of ABCA1 expression in glomerular endothelial cells are not fully understood. In this study we investigated the effect of exendin-4 on ABCA1 in glomerular endothelial cells of diabetic kidney disease (DKD) and the possible mechanism. We observed a marked increase in glomerular lipid deposits in tissues of patients with DKD and diabetic apolipoprotein E knock-out (apoE-/-) mice by Oil Red O staining and biochemical analysis of cholesterol. We found significantly decreased ABCA1 expression in glomerular endothelial cells of diabetic apoE-/- mice and increased renal lipid, cholesterol, and inflammatory cytokine levels. Exendin-4 decreased renal cholesterol accumulation and inflammation and increased cholesterol efflux by up-regulating ABCA1. In human glomerular endothelial cells, GLP-1R-mediated signaling pathways (e.g. Ca2+/calmodulin-dependent protein kinase, cAMP/PKA, PI3K/AKT, and ERK1/2) were involved in cholesterol efflux and inflammatory responses by regulating ABCA1 expression. We propose that exendin-4 increases ABCA1 expression in glomerular endothelial cells, which plays an important role in alleviating renal lipid accumulation, inflammation, and proteinuria in mice with type 2 diabetes.

Association between the CYP1A2-164 A/C polymorphism and colorectal cancer susceptibility: a meta-analysis.

To date, epidemiological studies have assessed the association between CYP1A2-164 A/C polymorphism and colorectal cancer susceptibility. However, the results of these studies remained controversial. We aimed to examine the associations by conducting a meta-analysis of case-control studies. A total of 11 studies including 5,093 cases and 5,941 controls evaluated the association between the CYP1A2-164 A/C polymorphism and colorectal cancer susceptibility. No significantly associations were found in all genetic models (CC vs. AA: OR = 1.14, 95 % CI = 0.93-1.40; AC vs. AA: OR = 1.05, 95 % CI = 0.91-1.20; dominant model: OR = 1.08, 95 % CI = 0.95-1.24; recessive model: OR = 1.10, 95 % CI = 0.95-1.28). In the subgroup analysis by ethnicity or source of controls, there were still no significant associations detected in all genetic models. This meta-analysis suggested the CYP1A2-164 A/C polymorphism was not a risk factor for increasing colorectal cancer, further large and well-designed studies are needed to confirm these conclusions.

Quantitative assessment of the association between XPG Asp1104His polymorphism and bladder cancer risk.

Published data regarding the association between XPG Asp1104His polymorphism and bladder cancer risk remained controversial. This meta-analysis of literatures was performed to draw a more precise estimation of the relationship. We systematically searched PubMed, Embase, and Web of Science with a time limit of June 22, 2013. Summary odds ratios (ORs) with 95 % CIs were used to assess the strength of the association between XPG Asp1104His polymorphism and bladder cancer risk using random effects model. A total of eight case-control studies including 2,613 cases and 2,934 controls were included for analysis. Overall, no significant association was found between XPG Asp1104His polymorphism and bladder cancer susceptibility for CC vs. GG (OR = 1.12, 95 % CI = 0.74-1.69), GC vs. GG (OR = 1.12, 95 % CI = 0.86-1.46), the dominant model CC + GC vs. GG (OR = 1.08, 95 % CI = 0.85-1.38), and the recessive model CC vs. GC + GG (OR = 0.92, 95 % CI = 0.66-1.29). In the subgroup analysis, no significant associations were found in either Asian or non-Asian population. This meta-analysis suggested that XPG Asp1104His polymorphism was not associated with bladder cancer risk.

A pooled analysis of the ERCC2 Asp312Asn polymorphism and esophageal cancer susceptibility.

Published data regarding the association between the excision repair cross-complimentary group 2 (ERCC2) Asp312Asn polymorphisms and esophageal cancer susceptibility remained controversial. This meta-analysis of literatures was performed to assess the strength of association between the ERCC2 and esophageal cancer susceptibility using random effects model. We systematically searched PubMed, Embase and Web of Science with a time limit of September 15, 2013. Summary odds ratios (ORs) with 95 % confidence intervals (CIs) were used to assess the strength of association between the ERCC2 Asp312Asn polymorphism and esophageal cancer susceptibility using random effects model. A total of seven case-control studies including 1,831 cases and 2,728 controls were included for analysis. Overall, a significant association was found between ERCC2 Asp312Asn polymorphism and esophageal cancer susceptibility for GA vs. GG (OR = 1.20, 95 % CI = 1.03-1.40) and for the dominant model GA/AA vs. GG (OR = 1.18, 95 % CI = 1.03-1.35). However, the ERCC2 Asp312Asn polymorphism was a protective factor for AA vs. GA/GG (OR = 0.63, 95 % CI = 1.15-2.65) in esophageal squamous cell carcinoma. Our meta-analysis suggested that the ERCC2 Asp312Asn polymorphism might be associated with increased risk of esophageal adenocarcinoma and a protective factor for esophageal squamous cell carcinoma.

The APE1 Asp148Glu polymorphism and colorectal cancer susceptibility: a meta-analysis.

BACKGROUND: Published data regarding the association between the APE1 Asp148Glu polymorphism and colorectal cancer susceptibility remained controversial. This meta-analysis of literatures was performed to draw a more precise estimation of the relationship. MATERIALS AND METHODS: We systematically searched PubMed, Embase, and Web of Science with a time limit of August 19, 2013. Summary odds ratios (ORs) with 95% CIs were used to assess the strength of association between the APE1 Asp148Glu polymorphism and colorectal cancer susceptibility using random-effects model. RESULTS: A total of eight case-control studies including 2,597 cases and 3,063 controls were included for analysis. Overall, no significant associations were found between the APE1 Asp148Glu polymorphism and colorectal cancer susceptibility for GG vs TT (OR = 1.00, 95% CI = 0.73-1.36, p = 0.00 for heterogeneity), TG vs TT (OR = 1.17, 95% CI = 0.88-1.55, p = 0.00 for heterogeneity), the dominant model GG + TG vs TT (OR = 1.21, 95% CI = 0.91-1.60, p = 0.00 for heterogeneity) nor the recessive model GG vs TG + TT(OR = 0.95, 95% CI = 0.75-1.20, p = 0.02 for heterogeneity). In subgroup analysis, no significant associations were found in the Asian or Caucasian populations. CONCLUSION: This meta-analysis suggested that the APE1 Asp148Glu polymorphism was not associated with colorectal cancer susceptibility among Asians or Caucasians.

XPC Lys939Gln and Ala499Val polymorphisms in colorectal cancer susceptibility: a meta-analysis of case-control studies.

The XPC Lys939Gln and Ala499Val polymorphisms were likely to be involved with the development of colorectal cancer. However, there had been inconsistent reports of association. This meta-analysis of literatures was performed to draw a more precise estimation of the relationship. We systematically searched PubMed, Embase and Web of Science for relevant articles with a time limit of December 2012. The strength of association between the XPC Lys939Gln and Ala499Val polymorphisms and colorectal cancer susceptibility were assessed by odds ratio (OR) with the corresponding 95 % confidence interval (95 % CI). This meta-analysis including six case-control studies evaluated the associations between the two XPC polymorphisms (Lys939Gln, Ala499Val) and colorectal cancer susceptibility. For XPC Lys939Gln, no obvious associations were found for all genetic models [CC vs AA: OR (95 % CI) = 1.12 (0.94-1.32); CA vs AA: OR (95 % CI) = 1.08 (0.94-1.24); the dominant model: OR (95 % CI) = 1.09 (0.97-1.23); the recessive model: OR (95 % CI) = 1.07 (0.92-1.25)]. For XPC Ala499Val, no obvious associations were also not found for all genetic models [TT vs CC: OR (95 % CI) = 0.84 (0.65-1.10); CT vs CC: OR (95 % CI) = 1.00 (0.86-1.15); the dominant model: OR (95 % CI) = 0.98 (0.85-1.12); the recessive model: OR (95 % CI) = 0.87 (0.67-1.12)]. This meta-analysis suggested that both the XPC Lys939Gln and Ala499Val polymorphisms were not risk factors for increasing colorectal cancer.

Involvement of inflammation-related miR-155 and miR-146a in diabetic nephropathy: implications for glomerular endothelial injury.

BACKGROUND: MicroRNAs have been demonstrated to play an important role in the pathogenesis of diabetic nephropathy (DN). In this study, we investigated both the repertoire of miRNAs in the kidneys of patients with DN and their potential regulatory role in inflammation-mediated glomerular endothelial injury. METHODS: The miRNA expression profiling of the renal biopsy samples was performed by a microarray analysis; then, in situ hybridization and real-time polymerase chain reaction (PCR) were used to determine the localization and expression of two of the miRNAs significantly up-regulated in human DN kidney samples, miR-155 and miR-146a, in the kidney tissues from type 1 and type 2 DN rat models. Human renal glomerular endothelial cells (HRGECs) cultured under high-glucose conditions were transfected with miR-155 and miR-146a mimics, and the transforming growth factor (TGF)-ß1, tumor necrosis factor (TNF)-α, and nuclear factor (NF)-κB expressions were examined by western blot, real-time PCR, and an electrophoresis mobility shift assay. RESULTS: The expression of both miR-155 and miR-146a was increased more than fivefold in the kidney samples of the DN patients compared with the controls, and the miR-155 expression was closely correlated with the serum creatinine levels (R = 0.95, P = 0.004). During the induction and progression of the disease in type 1 and type 2 DN rat models, miR-155 and miR-146a were demonstrated to increase gradually. In vitro, high glucose induced the over-expression of miR-155 and miR-146a in the HRGECs, which, in turn, increased the TNF-α, TGF-ß1, and NF-κB expression. CONCLUSIONS: Taken together, these findings indicate that the increased expression of miR-155 and miR-146a in the DN patients and in the experimental DN animal models was found to contribute to inflammation-mediated glomerular endothelial injury.

A case of focal segmental glomerulosclerosis syndrome secondary to high-altitude polycythemia.

In recent years, focal segmental glomerulosclerosis has become the commonest cause of the nephrotic syndrome seen in adults. Secondary focal segmental glomerulosclerosis is observed when glomerular workload is increased. We report a case of focal segmental glomerulosclerosis with nephrotic syndrome secondary to high-altitude polycythemia (HAPC). Our case points out that for patients with focal segmental glomerulosclerosis, who presented with nephrotic syndrome secondary to HAPC, treatments for HAPC are crucial for the reduction of proteinuria and renal protection instead of glucocorticoid and immunosuppressive drugs.

Fabrication of bimetallic Ag@ZnO nanocomposite and its anti-cancer activity on cervical cancer via impeding PI3K/AKT/mTOR pathway.

INTRODUCTION: Bimetallic nanoparticles, specifically Zinc oxide (ZnO) and Silver (Ag), continue to much outperform other nanoparticles investigated for a variety of biological uses in the field of cancer therapy. This study introduces biosynthesis of bimetallic silver/zinc oxide nanocomposites (Ag@ZnO NCs) using the Crocus sativus extract and evaluates their anti-cancer properties against cervical cancer. METHODS: The process of generating bimetallic nanoparticles (NPs), namely Ag@ZnO NCs, through the utilization of Crocus sativus extract proved to be uncomplicated and eco-friendly. Various methods, such as UV-vis, DLS, FTIR, EDX, and SEM analyses, were utilized to characterize the generated Ag@ZnO NCs. The MTT assay was employed to assess the cytotoxic properties of biosynthesized bimetallic Ag@ZnO NCs against the HeLa cervical cancer cell line. Moreover, the impact of Ag@ZnO NCs on HeLa cells was assessed by examining cell survival, ROS production, MMP levels, and induced apoptosis. Through western blot analysis, the expression levels of the PI3K, AKT, mTOR, Cyclin D, and CDK proteins seemed to be ascertained. Using flow cytometry, the cancer cells' progression through necrosis and apoptosis, in addition to the cell cycle analysis, were investigated. RESULTS: Bimetallic Ag@ZnO NCs that were biosynthesized showed a high degree of stability, as demonstrated by the physicochemical assessments. The median size of the particles in these NCs was approximately 80-90 nm, and their zeta potential was -14.70 mV. AgNPs and ZnO were found, according to EDX data. Further, Ag@ZnO NCs hold promise as a potential treatment for cervical cancer. After 24 hours of treatment, a dosage of 5 µg/mL or higher resulted in a maximum inhibitory effect of 58 ± 2.9. The concurrent application of Ag/ZnO NPs to HeLa cells resulted in elevated apoptotic signals and a significant generation of reactive oxygen species (ROS). As a result, the bimettalic Ag@ZnO NCs treatment has been recognized as a chemotherapeutic intervention by inhibiting the production of PI3K, AKT, and mTOR-mediated regulation of propagation and cell cycle-regulating proteins. CONCLUSIONS: The research yielded important insights into the cytotoxic etiology of biosynthesized bimetallic Ag@ZnO NCs against HeLa cells. The biosynthesized bimetallic Ag@ZnO NCs have a significant antitumor potential, which appears to be associated with the development of oxidative stress, which inhibits the development of the cell cycle and the proliferation of cells. Therefore, in the future, biosynthesized bimetallic Ag@ZnO NCs may be used as a powerful anticancer drug to treat cervical cancer.

XRCC1 Arg194Trp and Arg280His polymorphisms in bladder cancer susceptibility: a meta-analysis.

The XRCC1 Arg194Trp and Arg280His polymorphisms were likely to be involved with the development of bladder cancer. However, there had been inconsistent reports of association. This meta-analysis of literatures was performed to draw a more precise estimation of the relationship. We systematically searched PubMed, Embase, and Web of Science for relevant articles with a time limit of April 25, 2013. Summary odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association between the two polymorphisms and bladder cancer susceptibility using a random-effects model. This meta-analysis including 14 case-control studies evaluated the associations between the two XRCC1 polymorphisms and bladder cancer susceptibility. Overall, for Arg194Trp, significant associations were found in TT versus CC (OR=1.78, 95% CI=1.12-2.82) and the recessive model (OR=1.71, 95% CI=1.11-2.65); for Arg280His, significant associations were also found in AG versus GG (OR=1.63, 95% CI=1.24-2.13) and the dominant model (OR=1.39, 95% CI=1.07-1.82). When stratified by ethnicity, in Asian population, significant associations were found for Arg194Trp polymorphism in TT versus CC (OR=2.99, 95% CI=1.48-6.06), the dominant model (OR=1.33, 95% CI=1.03-1.72) and the recessive model (OR=2.72, 95% CI=1.36-5.45), and for Arg280His in GA versus GG (OR=2.13, 95% CI=1.63-2.97), but no significant associations were found in no-Asian population. This meta-analysis suggested that XRCC1 Arg194Trp and Arg280His polymorphisms were risk factors for increasing bladder cancer in Asian population.

A meta-analysis of evidences on XPC polymorphisms and lung cancer susceptibility.

Published data regarding the association between the XPC polymorphisms and lung cancer susceptibility remained controversial. This meta-analysis was performed to draw a precise estimation of the relationship. We systematically searched PubMed, Embase, Elsevier, and Web of Science with a time limit of September 10, 2012. Summary odds ratios (ORs) with 95 % CIs were used to assess the strength of association between these polymorphisms and lung cancer susceptibility using random-effects model. This meta-analysis including 13 case-control studies evaluated the associations between three commonly XPC polymorphisms (Lys939Gln, Ala499Val, and PAT(-/+)) and lung cancer susceptibility. No significant associations were found between the three XPC polymorphisms and lung cancer susceptibility (for Lys939Gln polymorphism: CC vs AA, OR = 1.191, p = 0.033; AC vs AA, OR = 0.992, p = 0.762, the dominant model, OR = 1.028, p = 0.521; the recessive model, OR = 1.205, p = 0.022). For Ala499Val polymorphism: TT vs CC, OR = 1.195, p = 0.071; TC vs CC, OR = 1.146, p = 0.133; the dominant model, OR = 1.161, p = 0.086; the recessive model, OR = 1.123, p = 0.156. For PAT(-/+) polymorphism: +/+ vs -/-, OR = 1.094, p = 0.539; +/- vs -/-, OR = 0.925, p = 0.313; the dominant model, OR = 0.969, p = 0.725; the recessive model, OR = 1.135, p = 0.290. p = 0.004 for Bonferroni testing). Significant associations were also not found in the subgroup analysis for the three XPC polymorphisms. This meta-analysis suggested that the three XPC polymorphisms might not be risk factors for developing lung cancer.

APE1 Asp148Glu gene polymorphism and bladder cancer risk: a meta-analysis.

Published data regarding the association between the apurinic/apyrimidinic endonuclease 1 (APE1) Asp148Glu polymorphism and bladder cancer risk showed inconclusive results. This meta-analysis of literatures was performed to draw a more precise estimation of the relationship. We systematically searched PubMed, Embase, Elsevier and Springer for relevant articles with a time limit of Jan. 2012. The strength of association between APE1 Asp148Glu polymorphism and bladder cancer risk was assessed by odds ratio (OR) with the corresponding 95 % confidence interval (95 % CI) using the software STATA(version10.0).A total of 11 case-control studies including 4,292 cases and 4,761 controls based on the search criteria were included for analysis. Overall, for GG versus TT, the pooled OR was 0.952 (95 % CI = 0.778-1.166), for the the G allele carriers (TG + GG) versus homozygote TT, the pooled OR was 0.984 (95 % CI = 0.897-1.078). In the stratified analysis by ethnicity, significantly risks were not found among Asians for GG versus TT (OR = 0.469; 95 % CI = 0.162-1.357) nor (TG + GG) versus TT (OR = 0.921, 95 % CI = 0.742-1.143). Similarly, for non-Asians, significantly risks were also not found for GG versus TT (OR = 0.992; 95 % CI = 0.861-1.144) nor (TG + GG) versus TT (OR = 1.010, 95 % CI = 0.897-1.137). This meta-analysis suggested that the APE1 T1349G (Asp148Glu) polymorphism was not associated with bladder cancer risk among Asians nor non-Asians.

Cell therapy for neuropathic pain.

Neuropathic pain (NP) is caused by a lesion or a condition that affects the somatosensory system. Pathophysiologically, NP can be ascribed to peripheral and central sensitization, implicating a wide range of molecular pathways. Current pharmacological and non-pharmacological approaches are not very efficacious, with over half of NP patients failing to attain adequate pain relief. So far, pharmacological and surgical treatments have focused primarily on symptomatic relief by modulating pain transduction and transmission, without treating the underlying pathophysiology. Currently, researchers are trying to use cell therapy as a therapeutic alternative for the treatment of NP. In fact, mounting pre-clinical and clinical studies showed that the cell transplantation-based therapy for NP yielded some encouraging results. In this review, we summarized the use of cell grafts for the treatment of NP caused by nerve injury, synthesized the latest advances and adverse effects, discussed the possible mechanisms to inform pain physicians and neurologists who are endeavoring to develop cell transplant-based therapies for NP and put them into clinical practice.

Malignant rhabdoid tumor of the omentum in an adult male: a case report and literature review.

Malignant rhabdoid tumors (MRTs) are rare tumors with high mortality rates and poor prognoses. MRTs occur mainly in the central nervous system, kidneys, and soft tissues, but rarely in the omentum. MRTs occur more commonly in infants and children and less frequently in adults. Here, we report the first observed case of MRT in an adult omentum. A 35-year-old man with abdominal distension and pain was admitted to the emergency department. Previously, several hospitals considered patients with cirrhosis who had not received active treatment. Computed tomography and magnetic resonance imaging revealed diffuse omental thickening and massive ascites. The surgery was performed at our hospital, and the pathological diagnosis was MRT with a SMARCB1(INI-1) deletion. Postoperatively, his symptoms improved, and he underwent five cycles of chemotherapy. However, 6 months after surgery, the tumor developed liver metastases, and the patient subsequently died. Primary MRT of the greater omentum is rare, and its pathological diagnosis usually requires extensive clinicopathological evaluation of various differential diagnoses and an appropriate work-up to exclude other malignancies associated with SMARCB1 deletion. At the same time, the lack of specific signs of omental MRT and its rapid progression should alert clinicians.

Surgical Strategy and Prognosis of Pancreatic Neuroendocrine Tumors Based on Smart Medical Imaging.

It is imperative to seize the "golden rescue time" and implement new concepts and new skills in modern trauma rescue. Combining with the development background of smart medical image analysis, this topic focuses on surgical strategies and prognostic measures and studies a serious and difficult disease frequently occurring in middle-aged and elderly people: pancreatic neuroendocrine tumors. This article uses the comparative test method and sample collection method to collect the medical records of patients with neuroendocrine tumors diagnosed by pathology from July 2010 to January 2018 in the First Affiliated Hospital of X City and analyze the samples with gender and age. At the same time, routine tumor marker examination and the location of NEN in the digestive system were performed. The distribution analysis of EUS characteristics of neuroendocrine tumor mucosa in each site was performed after operation, and the analysis of survival-related factors was performed during postoperative follow-up. The experimental data showed that among the tumor causes, WHO tumor grade (p < 0.05) and whether the surgical method was R0 resection (p < 0.05) were associated with prognosis. However, factors such as gender, age, and functional status were associated with prognosis. It has successfully completed the subject of surgical strategy and prognosis of pancreatic neuroendocrine tumors based on smart medical image analysis.

SIRT6 promotes ferroptosis and attenuates glycolysis in pancreatic cancer through regulation of the NF-κB pathway.

Pancreatic cancer (PC) is a malignant tumor with high mortality worldwide. SIRT6 plays versatile roles in human cancers. However, SIRT6 has rarely been studied in PC. The purpose of the present study was to explore the function and potential mechanism of SIRT6 in PC. The expression of SIRT6 in PC tissues and cells was detected by reverse transcription-quantitative PCR and western blotting. The overall survival time was analyzed through the Kaplan Meier method. Cell viability was measured by the Cell Counting Kit-8 assay. The Fe2+ content, glucose uptake, lactic acid and ATP production were detected through the corresponding kits. ROS was evaluated using the DCFH-DA detection kit. Protein expression was assessed by immunohistochemistry or western blot analysis. In the present study, SIRT6 was lowly expressed in PC tissues and cells compared with normal tissues and cells. Moreover, the low expression of SIRT6 was associated with a poor prognosis in patients with PC. Upregulation of SIRT6 significantly promoted the ferroptosis and inhibited the glycolysis in PC cells. However, knockdown of SIRT6 resisted ferroptosis and increased glycolysis in PC cells. Further studies found that the activation of NF-κB could reverse the effect of SIRT6 on PC cells. In addition, overexpression of SIRT6 restrained the growth of xenografted tumors and suppressed the nuclear transcription of NF-κB in vivo. Collectively, the present study indicated that SIRT6 promoted ferroptosis and inhibited glycolysis through inactivating the NF-κB signaling pathway in PC. These findings suggested that SIRT6 may become a therapeutic target for PC.

The Role of Cholesterol Homeostasis in Diabetic Kidney Disease.

Considerable evidence has proved that disturbed cholesterol metabolism played a crucial role in diabetic kidney disease. Besides, massive cholesterol depositions were found in intrinsic renal cells of diabetic kidney disease patients and animal models, causing cytotoxicity and affecting renal function. Statins could alleviate cholesterol depositions, podocyte injury, and microalbuminuria of diabetic kidney disease. In this review, we summarized the process of disturbed cholesterol metabolism and discussed how it induced kidney dysfunction in diabetic kidney disease.