Abstract
Recently, both cancer-associated fibroblasts (CAFs) and autophagy have been proven to play an important role in tumor development, including bladder cancer (BCa). However, the real mechanisms remain largely unclear. Here, we reconstruct a mimic tumor microenvironment to explore the interaction between CAFs and the BCa cell line T24 using a coculture system. Autophagy in CAFs was induced or inhibited by rapamycin or siRNA, respectively. After coculture with CAFs, T24 cell proliferation, invasion, and aerobic glycolysis were tested in vitro. Rapamycin induced and siAtg5 inhibited autophagy in CAFs. Enhanced autophagy in CAFs promoted cell proliferation and invasion in T24 cells in vitro, while there was no significant difference between the autophagy-inhibited group and the controls. Lactate concentration was elevated in both rapamycin-treated and siAtg5-treated groups compared with the control group. In addition, the expression levels of MCT1, MCT4, HK2, SLC2A1, and MMP-9 were all increased in T24 cells in the autophagy-enhanced group. Our results indicated that CAFs could regulate BCa invasion and metabolic phenotypes through autophagy, providing us with new alternative treatments for BCa in the future.
Highlights
Bladder cancer (BCa) is the sixth most common malignancy in males and the ninth when both genders are included worldwide, with an age-standardized incidence rate of 9.0 for males and 2.2 for females [1]
Recent studies have reported that metabolic syndrome, herbs containing aristolochic acids, and pioglitazone treatment were associated with an increased risk of BCa [4,5,6]
We downregulated the expression of Atg5 in human foreskin fibroblast (hFF) cells by siRNA
Summary
Bladder cancer (BCa) is the sixth most common malignancy in males and the ninth when both genders are included worldwide, with an age-standardized incidence rate of 9.0 for males and 2.2 for females (per 100,000 persons/year) [1]. It causes an enormous economic burden, impairs patients’ life quality, and threatens victims’ survival when it invades the muscle. Even in those with a non-muscleinvasive disease, the BCa patients suffer from a high recurrence rate after surgical removal [2]. Despite advances in etiology seeking and therapeutic strategy, the real disease mechanisms and feasible prevention measures, as well as the long-term oncological outcomes, still remain limited
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