Autophagy and urothelial carcinoma of the bladder: A review

Chandrasekar, Thenappan; Evans, Christopher P.

doi:10.4111/icu.2016.57.s1.s89

Cited by 21 publications

(12 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been well-demonstrated that autophagy depends on Atg5/Atg7, which is associated with microtubule-associated protein LC3 truncation and lipidation and may originate directly from the ER membrane and other membrane organelles. ATG5 and ATG7 regulate the formation of autophagosomes, but they are separated from autophagosomes after the formation of autophagosomes 35 , 36 . Therefore, there is an upregulation in the expression of ATG5 and ATG7, but it may not be a positive correlation between the ATG5/ATG7 mRNA levels and the autophagosomes in the spatial-temporal distribution.…”

Section: Discussionmentioning

confidence: 99%

Fluid Shear Stress Promotes Autophagy in Hepatocellular Carcinoma Cells

et al. 2018

View full text Add to dashboard Cite

The autophagy in cancer cells is recognized as an essential hallmark of tumors, which can enhance cancer cell migration and invasion, and result in high incidence of tumor metastasis. The fluid shear stress (FSS) in tumor mechanical microenvironment plays a pivotal role in mediating the behaviors and functions of cells. In this study, the hepatocellular carcinoma cells were exposed to 1.4 dyn/cm2 FSS to explore whether FSS could induce autophagy. The results of TEM, Ad-mCherry-GFP labeled LC3B, and mRNA and protein expression of autophagy markers confirmed that FSS could induce autophagy in a time-dependent manner. Additionally, the inhibition of autophagy significantly downregulated the expression of PI3K, FAK and Rho GTPases, and attenuated the ability of cell migration, suggesting that FSS-induced autophagy depended on PI3K- FAK-Rho GTPases pathway. This study elucidated the role of FSS in inducing autophagy during tumor progression, which has emerged as a promising clinical strategy for cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

Fluid Shear Stress Promotes Autophagy in Hepatocellular Carcinoma Cells

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Autophagy is a constitutively active evolutionary conserved physiologic catabolic process that is maintained at a basal rate by cells throughout the body 16. Accumulating studies showed that autophagy protects some cancers against anticancer treatments.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA UCA1 targets miR-582-5p and contributes to the progression and drug resistance of bladder cancer cells through ATG7-mediated autophagy inhibition

Wu¹,

Ning³

et al. 2019

OTT

View full text Add to dashboard Cite

BackgroundRently, the incidence of bladder cancer has been on the rise. Accumulating researches have been conducted to clarify the molecular mechanisms and potential therapeutic targets of bladder cancer. The present study aims to explore the regulatory mechanism of the urothelial carcinoma-associated 1 (UCA1)-miR-582-5p-ATG7 axis in bladder cancer.MethodsQuantitative real-time polymerase chain reaction was used to detect mRNA level. Relative protein expression was detected by western blot. wound healing assay and transwell were used to determine migration and invasion of cells. in addtion, luciferase reporter assay and immunohistochemistry were performed.ResultsUCA1 expression was upregulated in bladder cancer tissues and cells, while the depletion of UCA1 by shRNA resulted in the suppression of cell proliferation, invasion, migration, and drug resistance. Further studies demonstrated that UCA1 could directly interact with miR-582-5p, and that there was an inverse correlation between miR-582-5p and UCA1. In addition, we found that ATG7 is a target of miR-582-5p and can be downregulated by either miR-582-5p overexpression or UCA1 knockdown. In particular, the autophagy is reduced when UCA1 shRNA is introduced. Moreover, the in vivo experiment further demonstrated the contribution of UCA1 in bladder cancer including tumor growth, invasion, and migration, and UCA1 knockdown can inhibit the aforementioned activities.ConclusionThese results provided evidence for a novel UCA1 interaction regulatory network in bladder cancer, that is, UCA1-miR-582-5p-ATG7-autophagy axis. Our study provides a new insight into the treatment of bladder cancer.

show abstract

“…Bladder urothelial carcinoma (BUC) is one of the most common malignant tumors of the urinary system and is characterized by rapid progression and a high rate of recurrence (1,2). BUC recurs in approximately 50% of patients after surgery, and the 5-year overall survival rate for patients who develop or present with metastatic disease is a dismal 6% (3).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of REDD1 Sensitizes Bladder Urothelial Carcinoma to Paclitaxel by Inhibiting Autophagy

Zeng

Liu

Cao

et al. 2018

Clinical Cancer Research

View full text Add to dashboard Cite

Regulated in development and DNA damage response-1 (REDD1) is a stress-related protein and is involved in the progression of cancer. The role and regulatory mechanism of REDD1 in bladder urothelial carcinoma (BUC), however, is yet unidentified. The expression of REDD1 in BUC was detected by Western blot analysis and immunohistochemistry (IHC). The correlation between REDD1 expression and clinical features in patients with BUC were assessed. The effects of REDD1 on cellular proliferation, apoptosis, autophagy, and paclitaxel sensitivity were determined both and Then the targeted-regulating mechanism of REDD1 by miRNAs was explored. Here the significant increase of REDD1 expression is detected in BUC tissue, and REDD1 is first reported as an independent prognostic factor in patients with BUC. Silencing REDD1 expression in T24 and EJ cells decreased cell proliferation, increased apoptosis, and decreased autophagy, whereas the ectopic expression of REDD1 in RT4 and BIU87 cells had the opposite effect. In addition, the REDD1-mediated proliferation, apoptosis, and autophagy are found to be negatively regulated by miR-22 , which intensify the paclitaxel sensitivity via inhibition of the well-acknowledged REDD1-EEF2K-autophagy axis. AKT/mTOR signaling initially activated or inhibited in response to silencing or enhancing REDD1 expression and then recovered rapidly. Finally, the inhibited REDD1 expression by either RNAi or miR-22 sensitizes BUC tumor cells to paclitaxel in a subcutaneous transplant carcinoma model REDD1 is confirmed as an oncogene in BUC, and antagonizing REDD1 could be a potential therapeutic strategy to sensitize BUC cells to paclitaxel. .

show abstract

Autophagy and urothelial carcinoma of the bladder: A review

Cited by 21 publications

References 49 publications

Fluid Shear Stress Promotes Autophagy in Hepatocellular Carcinoma Cells

Fluid Shear Stress Promotes Autophagy in Hepatocellular Carcinoma Cells

Long noncoding RNA UCA1 targets miR-582-5p and contributes to the progression and drug resistance of bladder cancer cells through ATG7-mediated autophagy inhibition

Inhibition of REDD1 Sensitizes Bladder Urothelial Carcinoma to Paclitaxel by Inhibiting Autophagy

Contact Info

Product

Resources

About