The role of p38 in irinotecan-induced DNA damage and apoptosis of colon cancer cells

Rudolf, Emil; Králová, Věra; Rudolf, Kamil; John, Stanislav

doi:10.1016/j.mrfmmm.2013.02.002

Cited by 23 publications

(18 citation statements)

References 30 publications

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“…Similarly to the other chemotherapeutics reviewed here, irinotecan exposure induces p38 MAPK activation in CRC: however, as it concerns the biological role of the p38 MAPK node, it still appears to be both dose and context-dependent. Indeed, studies on the SW620 CRC line revealed that, if on one hand, high CPT-11 dosage induces acute and short-lasting p38 MAPK activation leading to apoptosis mediated by mitochondria and caspases, low CPT-11 dosage also activates p38 MAPK in a delayed but sustained manner, with apoptosis occurring only in a fraction of cells and promoting overall cell-survival [39].…”

Section: Irinotecan Effects On the P38 Mapk Signaling Pathway In Crcmentioning

confidence: 99%

The p38 MAPK Signaling Activation in Colorectal Cancer upon Therapeutic Treatments

Pranteda¹,

Piastra²,

Stramucci³

et al. 2020

IJMS

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Pharmacological treatment of colorectal carcinoma currently proceeds through the administration of a combination of different chemotherapeutic agents. In the case of rectal carcinoma, radiation therapy also represents a therapeutic strategy. In an attempt at translating much-needed new targeted therapy to the clinics, p38 mitogen activated protein kinase (MAPK) inhibitors have been tested in clinical trials involving colorectal carcinoma patients, especially in combination with chemotherapy; however, despite the high expectations raised by a clear involvement of the p38 MAPK pathway in the response to therapeutic treatments, poor results have been obtained so far. In this work, we review recent insights into the exact role of the p38 MAPK pathway in response to currently available therapies for colorectal carcinoma, depicting an intricate scenario in which the p38 MAPK node presents many opportunities, as well as many challenges, for its perspective exploitation for clinical purposes.

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Section: Irinotecan Effects On the P38 Mapk Signaling Pathway In Crcmentioning

confidence: 99%

The p38 MAPK Signaling Activation in Colorectal Cancer upon Therapeutic Treatments

Pranteda¹,

Piastra²,

Stramucci³

et al. 2020

IJMS

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“…5,6) Activation of p38 MAPK was reported to initiate the signal for apoptosis of colon cancer cells. 7) Besides, p38 activation has been implicated in modulating apoptosis in PC12 and rat cerebellar granule cells. 8,9) A recent study also supported the fact that p38 was activated in neonatal rat cardiomyocytes subjected to ischemia and that inhibition of p38 evidently protected cardiac myocytes from apoptosis.…”

mentioning

confidence: 99%

Baicalin Attenuates Acute Myocardial Infarction of Rats <i>via</i> Mediating the Mitogen-Activated Protein Kinase Pathway

Liu

Fan

Shi

et al. 2013

Biological & Pharmaceutical Bulletin

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Baicalin is a bioactive ingredient from the herb and has possessed various pharmacological actions. The present study was performed to evaluate the cardioprotective potential of baicalin against myocardial infarction and explore the potential mechanism. Baicalin was intraperitoneally injected into the rats by the doses of 50, 100 and 200 mg/kg, respectively, once a day for 7 d and, 30 min after the last administration, the left coronary artery was ligated. Infarct size was measured to analyze the myocardial damage. Myocardial specific enzymes, including creatine kinase (CK), the MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase (LDH) and cardiac troponin T (cTnT) were determined with the colorimetric method. Evidence for myocardial apoptosis was detected by caspase-3 activity measurement and Western blot analysis. We also examined the protein levels of three major subgroups of mitogen-activated protein kinases (MAPKs), namely, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 by immuoblotting. Our results indicated that baicalin significantly reduced the infarct size and myocardial enzymes (CK, CK-MB, LDH and cTnT). Administration of baicalin also suppressed the activity and protein expression of caspase-3. Moreover, the protein level of phosphorylated ERK (p-ERK) was found to be evidently augmented while the phosphorylated JNK (p-JNK) and phosphorylated p38 (p-p38) were strikingly diminished in infarcted rats with baicalin treatment. These findings suggest that the baicalin's cardioprotection associates with mediation of MAPK cascades in acute myocardial infarction of rats.

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“…The DNA damage response is one molecular event that results in apoptosis, and consequently numerous anti-cancer agents induce a DNA damage response (14)(15)(16)(17)(18). Hirsutine, one of the major alkaloids in Uncaria species, exhibits an anti-metastatic effect in a murine breast cancer model (6) and has an anti-tumor effect on HER2 + breast cancer cells by inducing DNA damage (7).…”

Section: Discussionmentioning

confidence: 99%

Targeting the ataxia telangiectasia mutated pathway for effective therapy against hirsutine-resistant breast cancer cells

et al. 2016

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Abstract. The present authors have recently demonstrated that hirsutine, one of the major alkaloids in Uncaria species, promotes cell apoptosis by inducing DNA damage and suppresses metastasis of breast cancer cells. Despite its potent anti-cancer activity, certain types of human breast cancer cells exhibit resistance to hirsutine. To maximize the clinical utility of hirsutine therapy against breast cancer, it is critical to explore the underlying mechanism that protects hirsutine-resistant breast cancer cell lines. To identify potential targets for overcoming hirsutine-resistance, the present study investigated a library of kinase inhibitors in combination with hirsutine treatment in the hirsutine-resistant human breast carcinoma MCF-7 cell line. Amongst the 96 compounds tested, inhibitors of the ataxia telangiectasia mutated (ATM) pathway sensitized MCF-7 cells to hirsutine-induced cell death along with a sustained DNA damage response. This sensitization of MCF-7 cells to the hirsutine-induced DNA damage response by interfering with the ATM pathway did not require p53. Instead, radical oxygen species generation was significantly increased in hirsute and ATM inhibitor-treated MCF-7 cells. In conclusion, the present findings suggest the importance of the ATM pathway for optimizing the anti-cancer effect of hirsutine in breast cancer cells.

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The role of p38 in irinotecan-induced DNA damage and apoptosis of colon cancer cells

Cited by 23 publications

References 30 publications

The p38 MAPK Signaling Activation in Colorectal Cancer upon Therapeutic Treatments

The p38 MAPK Signaling Activation in Colorectal Cancer upon Therapeutic Treatments

Baicalin Attenuates Acute Myocardial Infarction of Rats <i>via</i> Mediating the Mitogen-Activated Protein Kinase Pathway

Targeting the ataxia telangiectasia mutated pathway for effective therapy against hirsutine-resistant breast cancer cells

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