Synergistic inhibition of GP130 and ERK signaling blocks chemoresistant bladder cancer cell growth

Li, Xuanhao; He, Shanshan; Tian, Ye; Weiß, Robert M.; Martín, Daniel

doi:10.1016/j.cellsig.2019.109381

Cited by 18 publications

(16 citation statements)

References 36 publications

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“…However, the key treatment strategies, such as surgical resection, radiotherapy and chemotherapy, exhibited few effects [24][25][26] in clinical practice. Targeted therapy becomes a promising therapeutic approach; therefore, it is critical to explore the appropriate therapeutic targets [27,28]. In this study, we identified the possible involvement of a member of kinesin family, named KIF3A, in the progression of bladder cancer.…”

Section: Discussionmentioning

confidence: 99%

Retracted: Kinesin family member 3A stimulates cell proliferation, migration, and invasion of bladder cancer cells in vitro and in vivo

Zhou

Zheng

et al. 2021

FEBS Open Bio

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Section: Discussionmentioning

confidence: 99%

Retracted: Kinesin family member 3A stimulates cell proliferation, migration, and invasion of bladder cancer cells in vitro and in vivo

Zhou

Zheng

et al. 2021

FEBS Open Bio

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“…Genome-based subtyping has revealed many oncogenic targets contributing to bladder cancer development, e.g., fibroblast growth factor receptor (FGFR), PI3K (phosphoinositid-3 kinase), Akt (serine/threonine kinase), and mTOR (mechanistic target of rapamycin) [ 3 ]. Abnormal activation of these pathways leads to survival and proliferation of tumor cells along with metastatic competence, angiogenesis, and therapy resistance [ 4 ]. One way of tackling bladder cancer is to inhibit mTOR, where anomalous interconnected signaling pathways converge [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Bladder Cancer Metastasis Induced by Chronic Everolimus Application Can Be Counteracted by Sulforaphane In Vitro

Justin

Rutz

Maxeiner

et al. 2020

IJMS

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Chronic treatment with the mTOR inhibitor, everolimus, fails long-term in preventing tumor growth and dissemination in cancer patients. Thus, patients experiencing treatment resistance seek complementary measures, hoping to improve therapeutic efficacy. This study investigated metastatic characteristics of bladder carcinoma cells exposed to everolimus combined with the isothiocyanate sulforaphane (SFN), which has been shown to exert cancer inhibiting properties. RT112, UMUC3, or TCCSUP bladder carcinoma cells were exposed short- (24 h) or long-term (8 weeks) to everolimus (0.5 nM) or SFN (2.5 µM), alone or in combination. Adhesion and chemotaxis along with profiling details of CD44 receptor variants (v) and integrin α and β subtypes were evaluated. The functional impact of CD44 and integrins was explored by blocking studies and siRNA knock-down. Long-term exposure to everolimus enhanced chemotactic activity, whereas long-term exposure to SFN or the SFN-everolimus combination diminished chemotaxis. CD44v4 and v7 increased on RT112 cells following exposure to SFN or SFN-everolimus. Up-regulation of the integrins α6, αV, and β1 and down-regulation of β4 that was present with everolimus alone could be prevented by combining SFN and everolimus. Down-regulation of αV, β1, and β4 reduced chemotactic activity, whereas knock-down of CD44 correlated with enhanced chemotaxis. SFN could, therefore, inhibit resistance-related tumor dissemination during everolimus-based bladder cancer treatment.

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“…Cell clumps were considered colonies if they were larger than or equal to fifty cells. Colonies were imaged and counted [ 33 ]. The effectiveness of the employed agents on cell survival was determined by using the survival rate calculation as previously described [ 31 ].…”

Section: Methodsmentioning

confidence: 99%

Knocking down claudin receptors leads to a decrease in prostate cancer cell migration, cell growth, cell viability and clonogenic cell survival

et al. 2021

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Prostate cancer is the most common solid organ malignancy in the United States, and has the highest probability of all cancers in becoming invasive. New molecular targets are needed to define and impede the growth and progression of advanced prostate cancers. Claudins (Cldns) are transmembrane proteins that regulate paracellular permeability and cell polarity, and their levels are elevated in many human cancers such as breast, ovarian, pancreatic, and prostatic cancers. Previously, we found that Cldn3 and Cldn4 are expressed in aggressive high-grade human prostate cancer specimens. We and others have shown that there are higher levels of Cldn3 and Cldn4 in metastatic human prostate cancer cells than in normal human prostate cells. The result of targeting Cldn3 and Cldn4 expression on the growth and viability of prostate cancer cells has not been elucidated. Human prostate cancer PC3 and LNCaP cells were transfected with Cldn3 or -4 small interfering RNAs (siRNAs). Cldn3/Cldn4 siRNA treatment resulted in a greater than 85% decrease in the protein levels of Cldn3 and Cldn4, which was accompanied by a 30–40% decrease in prostate cancer cell growth and a 60–65% reduction in cell viability. There was decreased cell migration with Cldn3 and Cldn4 siRNA in both PC3 and LNCaP cells and a 60–75% decrease in the number of clones when treated with siCldn3 or siCldn4 compared to control. Knocking down Cldn3/Cldn4 affects prostate cancer cell growth and survival and may have therapeutic implications.

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Synergistic inhibition of GP130 and ERK signaling blocks chemoresistant bladder cancer cell growth

Cited by 18 publications

References 36 publications

Retracted: Kinesin family member 3A stimulates cell proliferation, migration, and invasion of bladder cancer cells in vitro and in vivo

Retracted: Kinesin family member 3A stimulates cell proliferation, migration, and invasion of bladder cancer cells in vitro and in vivo

Bladder Cancer Metastasis Induced by Chronic Everolimus Application Can Be Counteracted by Sulforaphane In Vitro

Knocking down claudin receptors leads to a decrease in prostate cancer cell migration, cell growth, cell viability and clonogenic cell survival

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