Carbon nanofibers and carbon nanotubes sensitize prostate and bladder cancer cells to platinum-based chemotherapeutics.

Recent data suggest that carbon nanomaterials can act as antitumor agents themselves by increasing the efficiency of cytotoxic agents when applied in combination. Here, carbon nanofibers (CNFs) and multi-walled carbon nanotubes (CNTs) were investigated regarding their impact on cellular function, cellular uptake and ability to sensitize cancer cells of urological origin to the conventional chemotherapeutics cisplatin and carboplatin. CNFs and CNTs (1-200 microg/ml) showed a low to moderate impairment of cellular function with CNFs being more deleterious than CNTs.

Enhanced inhibition of bladder cancer cell growth by simultaneous knockdown of antiapoptotic Bcl-xL and survivin in combination with chemotherapy.

The overexpression of antiapoptotic genes, such as Bcl-xL and survivin, contributes to the increased survival of tumor cells and to the development of treatment resistances. In the bladder cancer cell lines EJ28 and J82, the siRNA-mediated knockdown of survivin reduces cell proliferation and the inhibition of Bcl-xL sensitizes these cells towards subsequent chemotherapy with mitomycin C and cisplatin. Therefore, the aim of this study was to analyze if the simultaneous knockdown of Bcl-xL and survivin might represent a more powerful treatment option for bladder cancer than the single inhibition of one of these target genes.

siRNA-mediated inhibition of antiapoptotic genes enhances chemotherapy efficacy in bladder cancer cells.

Background: The up-regulation of antiapoptotic B-cell CLL/lymphoma 2 (BCL2), BCL2-like 1 (BCLXL), X-linked inhibitor of apoptosis (XIAP) and survivin is one mechanism by which cancer cells develop resistance towards chemotherapeutics. Therefore, the knockdown of these four genes could sensitise bladder cancer (BCa) cells towards chemotherapy.

Materials And Methods: BCL2, BCLXL, XIAP and survivin were inhibited using siRNAs--either one target-alone or all four targets simultaneously--in EJ28 and J82 BCa cells.

Simultaneous siRNA-mediated knockdown of antiapoptotic BCL2, Bcl-xL, XIAP and survivin in bladder cancer cells.

Bladder cancer (BCa) represents the ninth most common malignancy worldwide. Despite intensive treatment with surgery and chemotherapy the prognosis for BCa patients particularly at advanced stages is poor. The ability to evade apoptosis is a hallmark of cancer cells.

Multitarget siRNA inhibition of antiapoptotic genes (XIAP, BCL2, BCL-X(L)) in bladder cancer cells.

Background: The knockdown of XIAP, BCL2 and BCL-X(L) by siRNAs represents a promising treatment option for bladder cancer (BCa) since the overexpression of antiapoptotic genes is often associated with tumor progression and treatment resistance.

Materials And Methods: EJ28 BCa cells were transfected with siRNAs--separately and combined--followed by analysis of target expression, viability, clonogenic survival, apoptosis and cell cycle. Furthermore, a possible chemosensitization by siRNA pretreatment was investigated.

Antisense-mediated inhibition of survivin, hTERT and VEGF in bladder cancer cells in vitro and in vivo.

Since cancer cells are characterised by multiple genetic alterations the single inhibition of one tumour- associated gene might not be sufficient as a therapeutic strategy. We examined the effects of a combined inhibition of survivin, human telomerase reverse transcriptase (hTERT) and vascular endothelial growth factor (VEGF) with antisense oligodeoxynucleotides (AS-ODNs) and small interfering RNAs (siRNAs) in EJ28 and 5637 bladder cancer (BCa) cells. Following verification of the uptake of intraperitoneally applied fluorescence-labelled AS-ODNs and siRNAs in subcutaneous BCa xenografts, the target-directed constructs were tested as single agents in SCID mice bearing subcutaneous EJ28.

Carbon nanotubes filled with a chemotherapeutic agent: a nanocarrier mediates inhibition of tumor cell growth.

Aim: In this paper, carbon nanotubes (CNTs) are presented as feasible carriers for carboplatin, a therapeutic agent for cancer treatment. The drug was introduced into CNTs to demonstrate that they are suited as nanocontainers and nanocarriers and can release the drug to initialize its medical virtue.

Method: The filling was accomplished by a wet-chemical approach after the CNTs were opened.

Synthetic nucleic acids as potential therapeutic tools for treatment of bladder carcinoma.

Objectives: Abnormal gene activation in human tumours including bladder cancers (bCAs) may cause altered proliferation, maturation, and apoptosis as well as development of resistance to therapeutic interventions. Therefore, silencing of abnormally activated genes appears to be a rational approach for specific target-directed and sensitising therapies.

Methods: Of the available strategies for gene silencing, antisense-based techniques have attracted much attention and are the focus of this review.

Functional analyses of C13orf19/P38IP in prostate cell lines.

Human C13orf19 was previously identified to be downregulated in prostate cancer (PCa) but its function is unknown to date. In the present study, C13orf19 mRNA expression was inhibited by siRNA transfection. Furthermore, a possible regulation by androgens and the previously postulated interaction with p38 MAP kinase (p38MAPK) was investigated.