Cisplatin-induced response of c-jun N-terminal kinase 1 and extracellular signal-regulated protein kinases 1 and 2 in a series of cisplatin-resistant ovarian carcinoma cell lines

Cui, Wei; Yazlovitskaya, Eugenia M.; Mayo, Matthew S.; Pelling, Jill C.; Persons, Diane L.

doi:10.1002/1098-2744(200012)29:4<219::aid-mc1004>3.0.co;2-d

Cited by 67 publications

(27 citation statements)

References 34 publications

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“…Specifically, aberrantly-active Stat3 promoted by hyperactive EGFR and Jaks and the EGFR-mediated Erk activity support the altered proliferation of the resistant cells. Contrary to our study and a previous report (Cui et al , 2000) that implicate Erk activity in cisplatin resistance, it is reported that Erk activation is important in the response of renal epithelial or mouse proximal tubule cells to cisplatin (Arany et al , 2004; Kim et al , 2005), and that the loss of Erk activity may promote cisplatin-resistance (Villedieu et al , 2006). Thus, the role of Erk in the cellular response or the lack thereof to cisplatin may be cell-type and context dependent.…”

Section: Discussioncontrasting

confidence: 99%

Hyperactive EGF receptor, Jaks and Stat3 signaling promote enhanced colony-forming ability, motility and migration of cisplatin-resistant ovarian cancer cells

et al. 2011

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We present evidence that the cisplatin-resistant human ovarian cancer lines, A2780S/CP1 (S/CP1), A2780S/CP3 (S/CP3), and A2780S/CP5 (S/CP5), derived by subjecting the sensitive A2780S ovarian cancer line to multiple rounds of cisplatin treatments followed by recovery and are resistant to 1, 3, and 5 μM cisplatin, respectively, have increased colony-forming ability and altered morphology that is consistent with enhanced motility, migration, and invasiveness in vitro. The malignant phenotype progresses with increasing resistance and is associated with hyperactive epidermal growth factor receptor (EGFR)/extracellular signal-regulated kinase (Erk)1/2 and Janus kinases (Jaks), aberrant Signal Transducer and Activator of Transcription (Stat) 3 activation promoted by EGFR and Jaks, and epithelial-mesenchymal transition (EMT) in vitro. Survivin and FLIP anti-apoptotic factors, vascular endothelial growth factor (VEGF), and matrix metalloproteinase activities are also elevated in the resistant cells. Accordingly, the ectopic expression of constitutively-active Stat3C in the sensitive A2780S cells diminished cisplatin sensitivity. The inhibition of EGFR or Stat3 activity repressed Survivin, VEGF and Vimentin expression and the colony-forming potential, viability, motility, and migration of the resistant cells, and sensitized them to cisplatin. Analysis of human ovarian cancer patients’ tumor tissues shows aberrantly-active EGFR and Stat3 that in certain cases correlate with Vimentin over-expression. Intra-peritoneal mouse xenograft studies revealed, compared to the sensitive A2780S line that had low tumor incidence restricted to the ovary, a high tumor incidence for the resistant S/CP3 and S/CP5 lines that formed tumor nodules at several locations on the small-intestine and colon, and which responded poorly to cisplatin, but were sensitive to concurrent treatment with cisplatin and EGFR or Stat3 inhibitor. Hyperactive EGFR signaling through Stat3 and the Jak-Stat3 activity together promote ovarian cancer progression to cisplatin resistance and therefore represent targets for preventing the development of cisplatin resistance and the recurrent disease during cisplatin therapy in ovarian cancer.

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Section: Discussioncontrasting

confidence: 99%

Hyperactive EGF receptor, Jaks and Stat3 signaling promote enhanced colony-forming ability, motility and migration of cisplatin-resistant ovarian cancer cells

et al. 2011

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“…Whereas MEK/ERK inhibition in ovarian cancer increases sensitivity to cisplatininduced cell death in sensitive and resistant cell lines [32,33], MEK inhibition in melanoma led to cisplatin sensitivity in one cell line but resistance in another [34]. Inhibition of this pathway in cervical carcinoma cells can lead to increased resistance to cisplatin but not to doxorubicin [35].…”

Section: Discussionsupporting

confidence: 77%

Differential sensitivity of chemoresistant neuroblastoma subtypes to MAPK-targeted treatment correlates with ERK, p53 expression, and signaling response to U0126

Eppstein

Sandoval

Klein

et al. 2006

Journal of Pediatric Surgery

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“…This apparent discrepancy might be due to a difference between the cancer cell lines used in the previous and present study. In other words, the selective ERK antagonism can either potentiate [24,33,[43][44][45][46] or prevent [28][29][30][31][32]45] cisplatin-induced toxicity depending on the tumor cell line used, indicating that cisplatin-triggered ERK could convey both cell death and survival signals in a cell type-dependent manner. Therefore, the outcome of combined cisplatin/AE treatment might at least partly depend on whether the AE-mediated ERK blockade is protective or damaging for the particular tumor cell line.…”

Section: Discussionmentioning

confidence: 99%

Aloe emodin decreases the ERK-dependent anticancer activity of cisplatin

Mijatović¹,

Maksimović‐Ivanić²,

Radovic³

et al. 2005

CMLS, Cell. Mol. Life Sci.

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The present study describes the ability of an anthraquinone derivative aloe emodin (AE) to reduce the cytotoxic activity of the platinum(II)-based anticancer agent cisplatin toward murine L929 fibrosarcoma and C6 glioma cell lines. The protective effect of AE was demonstrated by MTT and crystal violet assays for cell viability, and involved supression of cisplatin-induced apoptosis and necrosis, as assessed by lactate dehydrogenase release and flow cytometric analysis of DNA fragmentation or phosphatidylserine exposure. Cell-based ELISA and Western blot analysis revealed that AE abolished cisplatin-triggered activation of extracellular signal-regulated kinase (ERK) in tumor cells, while activation of c-Jun N-terminal kinase was not significantly altered. A selective blockade of ERK activation with PD98059 mimicked the protective effect of AE treatment in both tumor cell lines. Moreover, AE failed to protect tumor cells against the ERK-independent toxicity of the Pt(IV)-based complex tetrachloro(O,O-dibutyl-ethylenediamine-N,N'-di-3-propanoate)platinum(IV). Taken together, these data indicate that herbal anthraquinone AE can downregulate the anticancer activity of cisplatin by blocking the activation of ERK in tumor cells.

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Cisplatin-induced response of c-jun N-terminal kinase 1 and extracellular signal-regulated protein kinases 1 and 2 in a series of cisplatin-resistant ovarian carcinoma cell lines

Cited by 67 publications

References 34 publications

Hyperactive EGF receptor, Jaks and Stat3 signaling promote enhanced colony-forming ability, motility and migration of cisplatin-resistant ovarian cancer cells

Hyperactive EGF receptor, Jaks and Stat3 signaling promote enhanced colony-forming ability, motility and migration of cisplatin-resistant ovarian cancer cells

Differential sensitivity of chemoresistant neuroblastoma subtypes to MAPK-targeted treatment correlates with ERK, p53 expression, and signaling response to U0126

Aloe emodin decreases the ERK-dependent anticancer activity of cisplatin

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