Antitumor Effects of Imidazoquinolines in Urothelial Cell Carcinoma of the Bladder

Smith, Eric B.; Schwartz, Michael; Kawamoto, Hironori; You, Xin; Hwang, David H.; Liu, Huixian; Scherr, Douglas S.

doi:10.1016/j.juro.2007.01.112

Cited by 55 publications

(73 citation statements)

References 16 publications

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“…Several studies have demonstrated that cytokines such as type I IFN or cytotoxic T cells could participate in tumor destruction in vivo induced by imiquimod. Imiquimod can induce a profound tumordirected cellular immune response (17,36). Sullivan et al revealed that antitumorigenic effect of imiquimod is mediated by upregulation of local IFN-α levels (16).…”

Section: Discussionmentioning

confidence: 99%

“…imiquimod can induce direct apoptosis in various cancer cells (13,17,18,20). To investigate whether imiquimod induces apoptosis in prostate cancer cells, TRAMP-C2 cells were treated with 10 or 20 µg/ml of imiquimod for 48 h, stained with PI and Annexin V, and analyzed by flow cytometry.…”

Section: Imiquimod Induces Mitochondria-dependent Apoptosis In Prostamentioning

confidence: 99%

“…It also significantly suppressed in vivo tumor growth in a mouse model for orthotopic bladder cancer (21). Imiquimod also induced apoptosis and cytokines production In vitro and in vivo growth inhibition of prostate cancer by the small molecule imiquimod in various bladder cancer cell lines and effectively inhibited in vivo tumor growth (17). An imidazoquinoline also enhanced in vivo apoptosis and increased lymphocytic infiltration and proinflammatory cytokine production in a mouse model of renal cell carcinoma (22).…”

Section: Introductionmentioning

confidence: 98%

“…Antitumor effects of the imidazoquinolines family have been demonstrated in urogenital cancers including bladder cancer and renal cell carcinoma (17)(18)(19)(20)(21). Treatment with an imidazoquinoline (3M-011) downregulated c-Myc expression in bladder cancer cells and reduced its transcriptional activity (21).…”

Section: Introductionmentioning

confidence: 99%

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In vitro and in vivo growth inhibition of prostate cancer by the small molecule imiquimod

Han

Lee

Jeon

et al. 2013

International Journal of Oncology

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Abstract. Prostate cancer is the second leading cause of cancer death in men worldwide. In the present study, we examined in vitro and in vivo antitumor effect of the small molecule imiquimod, also known as a TLR7 agonist, against prostate cancer. Imiquimod inhibited the growth of mouse (TRAMP-C2) and human (PC-3) prostate cancer cells. Treatment with imiquimod induced cell cycle arrest at the G 2 /M phase in TRMPA-C2 cells, confirmed by the changes of G 2 /M checkpoint regulators such as reduction of cyclin B1 expression and increase of phospho-CDC2 and p21 in TRAMP-C2 cells treated with imiquimod. Flow cytometry and western blot analysis revealed that imiquimod induced direct apoptosis in TRAMP-C2 cells via a mitochondrial-dependent pathway. Intratumoral injection with imiquimod reduced significantly tumor growth and increased apoptotic cells in mice subcutaneously implanted with TRAMP-C2 cells. Our results indicate that imiquimod can be an alternative therapeutic for locally generated prostate cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Imiquimod Induces Mitochondria-dependent Apoptosis In Prostamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

In vitro and in vivo growth inhibition of prostate cancer by the small molecule imiquimod

Han

Lee

Jeon

et al. 2013

International Journal of Oncology

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“…It was shown in vitro that imiquimod can directly induce apoptosis of tumor cells using several skin and bladder cancer cells lines, as well as tumor tissue cultures [97][98][99][100][101]. For the skin cancer cell lines, it was demonstrated that this proapoptotic activity was independent of membrane-bound death receptors.…”

Section: Tumor Cellsmentioning

confidence: 99%

The Use of TLR7 and TLR8 Ligands for the Enhancement of Cancer Immunotherapy

et al. 2008

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After completing this course, the reader should be able to:1. Describe the subtypes of Toll-like receptor 7 and 8 agonists and their effect on the different components of the antitumor immune response.2. Argue why they are used as stand-alone immunotherapeutic agents.3. Evaluate their potential to improve current approaches of active and passive immunotherapy.This article is available for continuing medical education credit at CME.TheOncologist.com. CME CME ABSTRACT

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4‐Amino‐3‐acetylquinoline‐induced apoptosis of murine L1210 leukemia cells involves ROS‐mitochondrial‐mediated death signaling and activation of p38 MAPK

Jantová

Repicky

Letašiová

et al. 2008

Cell Biochemistry & Function

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Quinolines are known to be multitarget agents with a broad spectrum of biological activity. In a previous study, we showed that newly prepared 4-amino-3-acetylquinoline (AAQ) possesses strong anticancer activities. In this study, we investigated whether AAQ has cytotoxicity in murine L1210 leukemia cells. Results from cell proliferation assays showed that AAQ caused significant decrease in cell number in a dose-dependent manner. The cell death induced by AAQ appeared to involve apoptosis, based on evidence from apoptotic DNA fragmentation, flow cytometry, fluorescence microscopy, and Western blot analyses. We found that AAQ-treated cells had activated p38 MAPK and that apoptosis was processed through a reactive oxygen species (ROS)-dependent mitochondrial pathway. In summary, our results suggest that AAQ can induce apoptosis, at least in part, through the activation of the p38 MAPK pathway in L1210 leukemia cells.

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Antitumor Effects of Imidazoquinolines in Urothelial Cell Carcinoma of the Bladder

Cited by 55 publications

References 16 publications

In vitro and in vivo growth inhibition of prostate cancer by the small molecule imiquimod

In vitro and in vivo growth inhibition of prostate cancer by the small molecule imiquimod

The Use of TLR7 and TLR8 Ligands for the Enhancement of Cancer Immunotherapy

4‐Amino‐3‐acetylquinoline‐induced apoptosis of murine L1210 leukemia cells involves ROS‐mitochondrial‐mediated death signaling and activation of p38 MAPK

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