Temsirolimus improves cytotoxic efficacy of cisplatin and gemcitabine against urinary bladder cancer cell lines

Pinto‐Leite, Rosário; Arantes‐Rodrigues, Regina; Ferreira, Rita; Palmeira, Carlos; Colaço, Aura; Silva, Vítor Moreira da; Oliveira, Paula A.; Santos, Lúcio Lara

doi:10.1016/j.urolonc.2013.04.012

Cited by 26 publications

(19 citation statements)

References 52 publications

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“…In contrast, in the T24 cell line, the addition of everolimus or temsirolimus to cisplatin did not increase the efficacy of the latter one but, when combined to gemcitabine resulted in enhanced cell proliferation inhibition. [40][41][42][43] This evidence supports the role of complex tumor signaling pathways in tumor behavior and response to chemotherapy and highlights the diverse and sometimes controversial results observed in preclinical studies.…”

Section: Ubc Cell Linessupporting

confidence: 70%

What we have learned from urinary bladder cancer models

Bernardo¹,

Costa²,

Palmeira³

et al. 2015

J Cancer Metastasis Treat

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Urinary bladder cancer (UBC) is a heterogeneous disease with highly variable clinical outcomes and responses to chemotherapy. Despite some advances in the molecular understanding of UBC, this knowledge still has not been translated to the clinic in terms of improvements in the prognosis and treatment of patients. Suitable urinary bladder tumor models representative of the human disease in terms of histology and behavior are needed to study factors involved in tumor initiation, progression and metastasis. Further, accurate model systems would facilitate identification of new therapeutic targets and predictive markers that could lead to optimization of existing therapies and development of new ones. Many established cancer cell lines derived from human urinary bladder tumors representing different grades and stages have been used as experimental models for UBC study. These cell lines reflect some of the genetic and morphologic alterations observed in human urothelial carcinoma and serve as simplified models to study the behavior of cancer cells in vitro. However, their translational potential is limited due to the artificial conditions, in which the cells are maintained, grown and tested. Animal models offer a more complex and realistic model for the establishment, development, and progression of tumors as well as to evaluate new therapeutic approaches. Over the years, the authors' group has worked with several UBC cell lines, established and characterized chemically induced UBC models, and patient-derived xenografts models. In this study, the authors will provide a summary of the UBC models developed by their group, analyze their translational potential and weaknesses, and define areas that remain to be explored.

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Section: Ubc Cell Linessupporting

confidence: 70%

What we have learned from urinary bladder cancer models

Bernardo¹,

Costa²,

Palmeira³

et al. 2015

J Cancer Metastasis Treat

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“…In addition, RA enhanced cisplatin effect through increasing sensitivity of resistant cells, which further activated their apoptosis. RA significantly inhibited proliferation by inducing S phase cell cycle arrest, whereas cisplatin induced cell cycle arrest at the G0/G1 stage [121]. The mRNA expression level of apoptotic genes was upregulated for p53 and Bax, whereas simultaneously led to a reduction of Bcl-2 and Survivin proteins [38].…”

Section: Hepatocellular Carcinoma (Hcc)mentioning

confidence: 96%

Anticancer Potential of Raddeanin A, a Natural Triterpenoid Isolated from Anemone raddeana Regel

et al. 2020

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Natural compounds extracted from plants have gained immense importance in the fight against cancer cells due to their lesser toxicity and potential therapeutic effects. Raddeanin A (RA), an oleanane type triterpenoid is a major compound isolated from Anemone raddeana Regel. As an anticancer agent, RA induces apoptosis, cell cycle arrest, inhibits invasion, migration and angiogenesis in malignant cell lines as well as in preclinical models. In this systemic review, the pharmacological effects of RA and its underlying molecular mechanisms were carefully analyzed and potential molecular targets have been highlighted. The apoptotic potential of RA can be mediated through the modulation of Bcl-2, Bax, caspase-3, caspase-8, caspase-9, cytochrome c and poly-ADP ribose polymerase (PARP) cleavage. PI3K/Akt signaling pathway serves as the major molecular target affected by RA. Furthermore, RA can block cell proliferation through inhibition of canonical Wnt/β-catenin signaling pathway in colorectal cancer cells. RA can also alter the activation of NF-κB and STAT3 signaling pathways to suppress invasion and metastasis. RA has also exhibited promising anticancer potential against drug resistant cancer cells and can enhance the anticancer effects of several chemotherapeutic agents. Overall, RA may function as a promising compound in combating cancer, although further in-depth study is required under clinical settings to validate its efficacy in cancer patients.

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“…The mTOR pathway is a regulator of the autophagic pathway. Pinto-Leite et al [ 47 ] utilized this fact to assess the efficacy of temsirolimus, a known mTOR inhibitor used for the treatment of other solid tumors, in conjunction with gemcitabine and cisplatin to 5637, T24, and HT1376 bladder cancer cell lines. Temsirolimus, in isolation, caused mild reduction in proliferation in a three cell lines, but in combination with gemcitabine or cisplatin, the effect was much more pronounced.…”

Section: Chemotherapymentioning

confidence: 99%

“…Temsirolimus, in isolation, caused mild reduction in proliferation in a three cell lines, but in combination with gemcitabine or cisplatin, the effect was much more pronounced. Though the increase in autophagic cells was mainly pronounced in the temsirolimus and cisplatin combination arm, there was a suggestion of autophagy induction and contribution to improved cytotoxicity [ 47 ].…”

Section: Chemotherapymentioning

confidence: 99%

Autophagy and urothelial carcinoma of the bladder: A review

Chandrasekar

Evans

2016

Investig Clin Urol

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The incidence of urothelial carcinoma of the urinary bladder (bladder cancer) remains high. While other solid organ malignancies have seen significant improvement in morbidity and mortality, there has been little change in bladder cancer mortality in the past few decades. The mortality is mainly driven by muscle invasive bladder cancer, but the cancer burden remains high even in nonmuscle invasive bladder cancer due to high recurrence rates and risk of progression. While apoptosis deregulation has long been an established pathway for cancer progression, nonapoptotic pathways have gained prominence of late. Recent research in the role of autophagy in other malignancies, including its role in treatment resistance, has led to greater interest in the role of autophagy in bladder cancer. Herein, we summarize the literature regarding the role of autophagy in bladder cancer progression and treatment resistance. We address it by systematically reviewing treatment modalities for nonmuscle invasive and muscle invasive bladder cancer.

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Temsirolimus improves cytotoxic efficacy of cisplatin and gemcitabine against urinary bladder cancer cell lines

Cited by 26 publications

References 52 publications

What we have learned from urinary bladder cancer models

What we have learned from urinary bladder cancer models

Anticancer Potential of Raddeanin A, a Natural Triterpenoid Isolated from Anemone raddeana Regel

Autophagy and urothelial carcinoma of the bladder: A review

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