The biological complexity of urothelial carcinoma: Insights into carcinogenesis, targets and biomarkers of response to therapeutic approaches

FGF9/FGFR2 increase cell proliferation by activating ERK1/2, Rb/E2F1, and cell cycle pathways in mouse Leydig tumor cells

“…Each FGF could interact with its specific FGFR to activate different signals in various cells, and studies have also shown that different FGF/FGFR signals participate in different cancer formations . Thus, the expressions of FGFR1‐4 regulated by FGF9 in MA‐10 cells were also investigated through western blot analysis.…”

“…Each FGF could interact with its specific FGFR to activate different signals in various cells, and studies have also shown that different FGF/ FGFR signals participate in different cancer formations. [7][8][9][10]66 Thus, the expressions of FGFR1-4 regulated by FGF9 in MA-10 cells were also investigated through western blot analysis. Results showed that 50 ng/ mL FGF9 could significantly increase the expression of FGFR1 at 12 hours of treatment, FGR2 at 48 hours of treatment, FGFR3 at 72 hours of treatment, and FGR4 at 48 hours of treatment ( Figure 6).…”

“…6 Thus, each FGF could interact with its specific FGFR to activate different signal pathways into cells. 7 Studies have shown that FGF/ FGFR signals participate in different cancer formations [8][9][10] : the abnormal or overexpression of FGFR1 could cause breast cancer and pancreatic adenocarcinoma, 11,12 the isoform switch of FGFR2 and splice mutation is involved in prostate cancer and gastric cancer, 13,14 the mutation, overexpression and aberrant splicing of FGFR3 participates in thyroid cancer, cervical cancer and colorectal cancer, [15][16][17] and the higher expression of FGFR4 Arg388 allele in head and neck carcinoma is associated with poor survival. 18 It is well known that FGFRs couple to tyrosine kinase receptors, which will transduce outer stimulation through PI3K, MAPK and phospholipase Cγ (PLCγ) pathways.…”

GP73 promotes invasion and metastasis of bladder cancer by regulating the epithelial–mesenchymal transition through the TGF‐β1/Smad2 signalling pathway

“…As there are no molecularly targeted agents approved for treating bladder cancer, The Cancer Genome Atlas (TCGA) project was conducted to identify potential therapeutic targets for this disease [29]. There is evidence supporting the fact that developments in molecular biology, genomics, bioinformatics and immunology may provide a solid foundation for therapeutic advances in treating this disease [30]. Therefore, the aim of this study was to investigate how GP73/ TGF-b1/Smad2 regulates the EMT and promotes the invasion and metastasis of bladder cancer.…”

The role of molecular genetic alterations in sensitivity of the adjuvant intravesical therapy for non-muscle invasive bladder cancer

“…Для МИРМП на начальных этапах свойственны мутации в генах ремоделирования хроматина и сегрегации хроматид (ARID1A, UTX, KDM6A, EP300, ESPL1 и др. ), что приводит к множественным одномоментным хромосомным перестройкам -хромотрипсису -и дальнейшему нарастанию геномной нестабильности, при этом отмечают высокую частоту мутаций ТР53 и RB1 [55,56]. На основании морфологических и иммуногистохимических характеристик, мутаций и профилей экспрессии генов выделяют подгруппы РМП, имеющие прогностическое значение: базальный, люминальный, р53-подобный и др., а также молекулярные профили TCGA (The Cancer Genome Atlas) -4 подтипа РМП.…”