Publications by authors named "Ganggang Jiang"

Background: Over the years, there has been extensive exploration of the association between testosterone and lipid profiles, yet the precise mechanisms underlying their interaction remain incompletely elucidated. Similarly, there is a dearth of research on the correlation between serum apolipoprotein B (apoB) and serum total testosterone (TT), particularly within specific populations.

Methods: We conducted a cross-sectional study to assess the relationship between serum TT concentration and serum apoB concentration.

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Rheumatoid arthritis (RA) is a persistent systemic autoimmune disease with the hallmarks of swelling of the joint, joint tenderness, and progressive joint destruction, which may cause synovial inflammation and pannus as a basic pathological change, resulting in joint malformations and serious disorders. At present, the precise etiology and mechanism of pathogenesis of RA are unknown. The imbalance of immune homeostasis is the origin of RA.

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Rheumatoid arthritis (RA) is a persistent systemic autoimmune disease, having all the hallmarks of joint swelling, joint tenderness, and progressive joint destruction, with synovitis and pannus formation as the basic pathological changes. T-lymphocyte infiltration is the key to its pathogenesis. During the growth of RA, the share of regulatory T (Treg) cells decreases, while the percentage of T helper type 17 (Th17) cells increases, giving rise to an imbalance of Th17/Treg cells.

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Oxidative stress induced by high glucose (HG) plays an important role in the mechanism of diabetic cataract. Evidence has shown that effects from oxidative stress induced damage of lens or human lens epithelial (HLE) cells. Antioxidant supplementation is a plausible strategy to avoid oxidative stress and maintain the function of lens.

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Accumulated evidence shows that complex microbial communities resides in the healthy human urinary tract and can change in urological disorders. However, there lacks a comprehensive profiling of the genitourinary microbiota in healthy cohort. Here, we performed 16S rRNA gene sequencing of midstream urine specimens from 1,172 middle-aged and elderly healthy individuals.

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Prostate cancer (PCa) is one of the most frequently diagnosed malignancy. Although there have been many advances in PCa diagnosis and therapy, the concrete mechanism remains unknown. Long non-coding RNAs (lncRNAs) are novel biomarkers associated with PCa, and their dysregulated expression is closely associated with risk stratification, diagnosis and carcinogenesis.

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Prostate cancer poses a public health threat to hundreds of people around the world. p62 has been identified as a tumor suppressor, however, the mechanism by which p62 promotes prostate cancer remains poorly understood. The present study aimed to investigate whether p62 promotes proliferation, apoptosis resistance and invasion of prostate cancer cells via the Kelch‑like ECH‑associated protein 1/nuclear factor erytheroid‑derived 2‑like 2/antioxidant response element (Keap1/Nrf2/ARE) axis.

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MicroRNAs (miRNAs or miR) serve as oncogenes and tumor suppressors. In a previous study, it was revealed that has-miRNA-429 (miR-429) is a tumor suppressor in 786-O renal cell carcinoma (RCC) cells. However, its mechanism in RCC remains to be determined.

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Pentatricopeptide repeat domain protein 3 (PTCD3) is a mitochondrial RNA‑binding protein that serves a role in mitochondrial translation. PTCD3 was originally reported as an oncogene that is involved in breast cancer and lymphoma. However, the expression and function of PTCD3 in prostate cancer (PCa) are unknown.

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With increases in the mortality rate and number of patients with prostate cancer (PCa), PCa, particularly the advanced and metastatic disease, has been the focus of a number of studies globally. Over the past seven decades, androgen deprivation therapy has been the primary therapeutic option for patients with advanced PCa; however, the majority of patients developed a poor prognosis stage of castration resistant prostate cancer (CRPC), which eventually led to mortality. Due to CRPC being incurable, laboratory investigations and clinical studies focusing on CRPC have been conducted worldwide.

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Background: P62 (also named sequestosome-1, SQSTM1) is involved in autophagy regulation through multiple pathways. It interacts with autophagosomes-associated LC3-II and ubiquitinated protein aggregates to engulf the aggregates in autophagosomes, interacts with HDAC6 to inhibit its deacetylase activity to maintain the levels of acetylated α-tubulin and stabilities of microtubules to enhance autophagosome trafficking, and regulates autophagy initiation and cell survival. We performed immunohistochemistry staining of P62 in prostate tissues from prostate cancer patients and found that levels of P62 in patients with prostate adenocarcinomas (PCA) are significantly higher than those in patients with benign prostate hyperplasia (BPH).

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