The biological characteristics of bladder cancer include enhanced invasion and migration, which are the main causes of death in patients. Starvation is a typical feature of the bladder cancer microenvironment and can induce autophagy. Autophagy has an important relationship with the invasion and migration of tumors. However, the role of autophagy in the invasion and migration of bladder cancer cells remains unclear. Hence, the aim of the current study was to clarify this role and underlying mechanism. In this study, we found that starvation enhanced the epithelial‐mesenchymal transition (EMT)‐mediated invasion and migration of T24 and 5637 cells while inducing autophagy. The inhibition of autophagy with chloroquine (CQ) or 3‐methyladenine (3MA) decreased EMT‐mediated invasion and migration. In addition, the expression of transforming growth factor 1 (TGF‐β1) and phosphorylated Smad3 (p‐Smad3) increased after starvation. The inhibition of autophagy with CQ or 3MA also decreased the expression of TGF‐β1 and p‐Smad3. The inhibitor of TGF‐β receptor sb431542 also inhibited the invasion, migration, and EMT of T24 and 5637 cells during starvation. Furthermore, recombinant TGF‐β1 induced autophagy and inhibition of the TGF‐β/Smad signaling pathway with sb431542 suppressed autophagy. In summary, our results suggested that autophagy promotes the invasion and migration of bladder cancer cells by inducing EMT through the TGF‐β1/Smad3 signaling pathway. Moreover, autophagy and TGF‐β1 can form a positive feedback loop to synergistically promote invasion and migration. Thus, our findings may provide a theoretical basis for the prevention of invasion and migration in bladder cancer.
The role of autophagy in the anticancer activity of gemcitabine (GEM) in bladder cancer is unclear. The aim of this study is to determine whether GEM activates autophagy, the role of autophagy in the anticancer activity of GEM, and the underlying mechanism by which GEM induces autophagy. Human bladder cancer cell lines T24 and BIU87 were treated with GEM in vitro. Cell viability was measured using the Cell Counting Kit-8 assay. Apoptosis was detected by annexin V assay and western blot. Autophagy was measured by western blot and transmission electron microscopy. c-Jun N-terminal kinase (JNK) activation was detected by western blot. Chemical inhibitors were used for intervention of JNK and autophagy. GEM killed bladder cancer cells, which was associated with apoptosis induction. Autophagy was effectively activated by GEM. Suppressing autophagy in GEM-treated cells significantly decreased cell viability, which was associated with increased apoptosis. GEM-induced JNK activation and suppressed B-cell lymphoma 2 expression. The JNK inhibitor SP600125 inhibited GEM-induced autophagy activation and increased GEM's cytotoxicity. GEM kills bladder cancer cells through apoptosis. Meanwhile, JNK-mediated autophagy was activated, which protects the cells against apoptosis. Therefore, inhibition of autophagy could be exploited to enhance the anticancer efficacy of GEM for treating bladder cancer.
Cystadenomas of the seminal vesicles are extremely rare. Here, we report a large seminal vesicle cystadenoma. A 37‐year‐old man presented a 6‐month history of haemospermia, 10 days of Lower Urinary Tract symptoms (LUTSs) and gross haematuria. Transabdominal ultrasonography, computed tomography and magnetic resonance imaging were performed and revealed a large solid‐cystic pelvic mass morphometrically measured 7.0 cm × 11.9 cm × 8.6 cm on the right seminal vesicle, which caused hydronephrosis of the right kidney. The prostate‐specific antigen of the patient was 27.860 ng/dl. Laparoscopic exploration found the capsule of tumour was complete and the tumour came from the right seminal vesicle, in addition, the mass had a certain space with the bladder and prostate, which could be separated. So a nerve‐sparing Laparoscopic Vesiculectomy was performed at last, even though the intraoperative frozen section analysis could not make sure the nature of the tumour either. The postoperative pathology revealed cystadenoma of the seminal vesicle.
XP11.2 translocation TFE3 gene fusion renal cell carcinoma (RCC) is enlisted as a rare subtype of RCC by WHO in 2004. This type of Tumor was previously considered a pediatric tumor predominantly but is now invariably found in adult and older patients. The article investigates the clinical manifestation, pathological features, diagnosis criteria, and treatment of this rare subtype of RCC. We collected the clinical data of eight patients confirmed as XP11.2 TFE3 RCC admitted in the First affiliated hospital of Chongqing Medical University from August 2015 to November 2018, and a retrospective analysis of these data was conducted. There were three male, five female patients, the average age of 33.25 years old, ranging from 5 years old to 62. Six patients were asymptomatic and diagnosed incidentally, one of them complained of hematuria and back pain for three months, and another patient complained just back pain for four months. After hospital admission, transabdominal ultrasonography, CT scan, and MRI imaging were done on all the patients. The tumor sizes of 2 patients were more than 7cm; 3 patients were 5-6 cm, and the rest three patients were below 4cm. One Patient got an Open Radical Nephrectomy for the right kidney and Right Ureterectomy. Four patients went through a Radical nephrectomy, and partial nephrectomies were done in the rest three patients. All the removed tumor samples were analyzed using pathology and immunohistochemistry assays. The results showed that all samples had renal carcinoma cells, with positive CD10 and TFE3 staining. Other parameters varied from each other. One postoperative Patient got both chemotherapies and targeted therapy; 3 patients were treated with Interferon but changed to thymopentin due to adverse effects. Only one Patient got thymopentin, and the rest three patients did not need any adjuvant therapy. Follow-up was done on all patients from 6 months to 40 months. Except for one patient who died of lung metastasis at 16 months after surgery, no disease progression occurred in those patients. The imaging findings are atypical, constantly varying among different patients with various tumor morphologies. So far, the golden standard of diagnosis is postoperative pathology and immune histochemistry. Radical or partial nephrectomy combining with renal lymph node clearance should be performed if metastasis of lymph nodes occurs. Proper adjuvant therapy, including chemotherapies, targeted therapy, and immune therapy, should be applied when needed. To maintain a risk-free life, follow-up must be done every 3 to 6 months.
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