The combination of docetaxel and the somatostatin analogue lanreotide on androgen‐independent docetaxel‐resistant prostate cancer: experimental data

Nigro, Cristiana Lo; Maffi, Monica; Fischel, Jean‐Louis; Formento, Patricia; Milano, Gérard; Merlano, Marco

doi:10.1111/j.1464-410x.2008.07706.x

Cited by 35 publications

(30 citation statements)

References 20 publications

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“…In contrast, the cytotoxic radical and the carrier protein, administered separately, were ineffective and toxic (68). In line with these data, a recent in vitro study reported that lanreotide could interact with docetaxel in HRPCa cells, with possible explanatory mechanisms involving the regulation of the interaction of P-glycoprotein-mediated docetaxel through lanreotide (69). This latter evidence was corroborate by the same authors which also demonstrated that octreotide and docetaxel combination increase HRPCa cell death through cell cycle regulation and induction of apoptosis (70).…”

Section: Somatostatin Analogues and Prostate Cancersupporting

confidence: 79%

Somatostatin and prostate cancer: role of somatostatin receptors in the control of tumor growth

Arvigo¹,

Ruscica²,

Albertelli³

et al. 2013

REM

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SummaryThe evidence that prostate cancer (PCa) expresses specific receptors for hormones and neuropeptides, including somatostatin (SRIF) receptors (SSRs) has driven the research towards the identification of new potential diagnostic/therapeutic paths besides the conventional treatment options. Although the first attempts has led to inconclusive results due to the heterogeneity of this tumor and to the complex mechanisms involved in the progression of PCa tumor growth, the potential role of SRIF and its synthetic analogues (SSAs) in the treatment of PCa represents an "open challenge" in the light of the new knowledge about SSR pathophysiology. Indeed, SRIF and SSAs can control tumor cell proliferation by two separate mechanisms: a direct mechanism through the activation of the five specific SSRs or an indirect mechanism through the inhibition of secretion of several growth factors and hormones responsible for tumor cell proliferation. Since new SSAs specific for each receptor subtype, as well as bi-specific compounds and panligands have been synthetized, the identification of alternative SSR targets on PCa cells and the consequent employment of these new specific molecules in the treatment of advanced PCa (alone or in combination with traditional treatment options), could improve the prognosis particularly of those patients not responding to (anti-) hormonal therapy (hormone-refractory PCa patients).

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Section: Somatostatin Analogues and Prostate Cancersupporting

confidence: 79%

Somatostatin and prostate cancer: role of somatostatin receptors in the control of tumor growth

Arvigo¹,

Ruscica²,

Albertelli³

et al. 2013

REM

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“…Interestingly, other PC3-derived docetaxel-resistant cell lines have been reported with widely varying degrees of resistance. The reported resistance factor ranged from 4 to 400 nmol/L (20). The LDocR cells used in our report therefore represent a moderately resistant derived cell line, with just a >10-fold increase in the GI 50 value for docetaxel along with increased MDR1 activity (Fig.…”

Section: Discussionmentioning

confidence: 98%

Docetaxel-Resistant Prostate Cancer Cells Remain Sensitive toS-Trityl-l-Cysteine–Mediated Eg5 Inhibition

Wiltshire

Singh

Stockley

et al. 2010

Molecular Cancer Therapeutics

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Castrate-resistant prostate cancer remains a major clinical challenge. Due to the toxicity profile of taxane-based chemotherapy and treatment failure in some patients, novel agents with improved efficacy to side effect profiles are urgently needed. Eg5, a member of the kinesin-5 family, controls the formation of the bipolar spindle during cell division, and suppressed Eg5 function leads to mitotic arrest. S-Trityl-Lcysteine (STLC) is a novel Eg5-specific small-molecule inhibitor. Here, we report the first study to evaluate its use in prostate cancer. In a panel of prostate cancer cells, LNCaP and PC3 cells were the most and least sensitive to STLC treatment, with a 7.2-fold difference in their respective GI 50 values: 250 nmol/L and 1.8 μmol/L. In LNCaP cells, treatment with either STLC or docetaxel resulted in transient G 2 -M arrest and subsequent caspase-mediated cell death. However, STLC-and docetaxel-treated PC3M cells have distinct fates: STLC induced a transient G 2 -M arrest, followed by polyploidy; in contrast, docetaxel-treated PC3M cells progressed to apoptosis after a transient G 2 -M arrest. Docetaxel-resistant LNCaP-derived (LDocR) cells respond to STLC in a similar manner to the parental cells. Although the docetaxel-resistant PC3M-derived (PDocR) cell line and its parental PC3M cells have similar GI 50 to STLC treatment, PDocR cells showed significantly more G 2 -M arrest and less apoptosis. Hence, although docetaxel-resistant prostate cancer cells remain responsive to Eg5 inhibition with STLC, there are key differences at the cell cycle level, which may have implication in future development.

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“…We first established the docetaxel-resistant PC3 (PC3R) using the method evaluated by the previous report [11] . PC3 cells were made resistant to docetaxel by culturing them under continuous exposure to docetaxel (10 nmol/L) for 30 days.…”

Section: Exposure To Docetaxel and Ic 50 Values Of Pc3wt And Pc3r Cellsmentioning

confidence: 99%

Involvement of microRNA-21 in mediating chemo-resistance to docetaxel in androgen-independent prostate cancer PC3 cells

et al. 2010

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Aim: To investigate whether microRNA-21 was involved in mediating the chemoresistance of prostate cancer cells to docetaxel. Methods: A microarray technique was used to determine the miRNA profile in docetaxel-resistant PC3 cells. Real-time PCR was used to confirm the array results. miR-21 mimics and inhibitors were synthesized and introduced to cells using Lipofectamine 2000. Cell proliferation was examined with the CCK-8 assay. Luciferase reporter containing PDCD 3′UTR was constructed and the activity was detected by a dual luciferase assay. PDCD4 protein expression was evaluated using Western blot. Results: A docetaxel-resistant prostate cancer PC3 cell line (PC3R) was established . Using microarrays, miR-21 was found to be upregulated in PC3R cells. Ectopic expression of miR-21 increased the resistance to docetaxel in PC3 wild type cells. In contrast, silencing of miR-21 in PC3R cells sensitized the cells to docetaxel. The IC 50 values for miR-21-silencing cells and control cells were 28.31 and 35.89 nmol/L, respectively. PDCD4, a direct target gene of miR-21, could mediate chemoresistance to docetaxel in PC3 cells. Conclusion: Our findings suggest that miR-21 contributed to the resistance of PC3 cells to docetaxel, and that targeting miR-21 may offer a promising therapeutic approach in sensitizing prostate cancer to docetaxel treatment.

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The combination of docetaxel and the somatostatin analogue lanreotide on androgen‐independent docetaxel‐resistant prostate cancer: experimental data

Cited by 35 publications

References 20 publications

Somatostatin and prostate cancer: role of somatostatin receptors in the control of tumor growth

Somatostatin and prostate cancer: role of somatostatin receptors in the control of tumor growth

Docetaxel-Resistant Prostate Cancer Cells Remain Sensitive toS-Trityl-l-Cysteine–Mediated Eg5 Inhibition

Involvement of microRNA-21 in mediating chemo-resistance to docetaxel in androgen-independent prostate cancer PC3 cells

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