Acute Peripheral Motor Neuropathy Induced by Oxaliplatin-Correlated Hypokalaemia

Maccaroni, Elena; Sotte, Valeria; Baleani, Maria Giuditta; Meletani, Tania; Giglio, Enrica; Pecci, Federica; Bittoni, Alessandro; Lanese, Andrea; Cantini, Luca; Mentrasti, Giulia; Lucarelli, Alessandra; Berardi, Rossana

doi:10.1007/s40487-019-00102-3

Cited by 3 publications

(1 citation statement)

References 27 publications

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“…The chemotherapeutic agents commonly used in CRC are 5-fluorouracil ( 5-FU) , oxaliplatin and irinotecan ( 2) . Although currently marketed chemotherapeutic agents are commonly used, their application is still limited due to drug resistance and serious side effects such as myelosuppression, peripheral neuropathy and hypokalemia (3,4). Therefore, new compounds with high anti-cancer and lower toxicity are extremely needed for CRC treatment.…”

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The roles of ROS and P21 in apoptosis-inducing effect of cepharanthine in human colorectal cancer cells

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Cepharanthine (CEP), a natural compound isolated from Stephania cepharantha Hayata, has been shown to possess anti-cancer activity against several cancers including colorectal cancer (CRC) cells. Previously, it was found that cytotoxicity of CEP was associated with ROS generation and p21Waf1/Cip1 expression. However, information regarding to the molecular mechanisms underlying the apoptosis-inducing effects of CEP in CRC cells is still limited. Therefore, the present study aimed to evaluate the roles of ROS and p21Waf1/Cip1 in the apoptosis-inducing effect of CEP in two human colorectal cancer cells lines, p53 wild-type HCT116 cells and p53 mutant HT-29 cells. The results demonstrated that CEP significantly inhibited the growth of both HT-29 and HCT116 cells. Remarkably, CEP was more effective than L-OHP in controlling the growth of HT-29 cells. Moreover, CEP induced apoptosis was mediated through upregulation of pro-apoptotic Bak, downregulation of anti-apoptosis Bcl-xL, and induction of poly (ADP-ribose) polymerase (PARP) cleavage in both HT-29 cells and HCT116 cells. Additionally, CEP was found to induce ROS generation in HT-29 and HCT-116 cells. It should be noted that N-acetyl cysteine (NAC) could abolish the apoptosis-inducing effects of CEP in both HT-29 cells and HCT116 cells, suggesting that CEP-induced apoptosis is mediated through ROS generation. Furthermore, CEP could modulate ERK1/2 signaling pathway by inhibiting ERK1/2 phosphorylation in HT-29 cells while activating ERK1/2 phosphorylation in HCT116 cells, which was found to be associated with ROS generation. Notably, CEP markedly upregulated the expression of p21Waf1/Cip1 in p53 mutant HT-29 cells but did not alter the expression of p21Waf1/Cip1 in HCT116 cells. A p21 inhibitor, UC2288, could abolish apoptosis-inducing effect of CEP in HT-29 cells, suggesting that CEP-induced apoptosis is mediated via upregulation of p21Waf1/Cip1 in p53 mutant HT-29 cells. Taken together, the results of this study demonstrated that generation of ROS and upregulation of p21 Waf1/Cip1 play a significant role in apoptosis-inducing effect of CEP in p53 mutant CRC cells. It may be useful for treatment of colorectal cancer carrying mutant p53 which often cause resistant to current chemotherapeutic agents.

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The roles of ROS and P21 in apoptosis-inducing effect of cepharanthine in human colorectal cancer cells

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Capecitabine/glucose/oxaliplatin

2020

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FOLFOX regimen induced severe hypokalaemia with hypocalcaemia and hypomagnesaemia

Mahadevappa,

Krishnamurthy,

Hussain

et al. 2024

BMJ Case Rep

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FOLFOX regimen is a chemotherapy regimen commonly used to treat colorectal cancers and other gastrointestinal malignancies. It comprises a combination of drugs, including leucovorin, 5-fluorouracil and oxaliplatin. Hypokalaemia can be a potential adverse drug reaction to the FOLFOX regimen, along with other haematological or metabolic adverse effects. Causes for hypokalaemia include chemotherapy-induced diarrhoea, nausea, vomiting and increased renal loss of potassium. The oxaliplatin used in the FOLFOX regimen is often associated with hypokalaemia due to intracellular shift, secondary to using 5% dextrose for infusion. Therefore, close monitoring of electrolyte levels, including potassium, is essential during chemotherapy treatment. Patients may require supplementation with potassium, either orally or intravenously, to maintain adequate levels and prevent complications. Additionally, managing diarrhoea, nausea and vomiting can help minimise potassium loss during chemotherapy. This case describes a patient who developed severe hypokalaemia (1.4 mmol/L) associated with the use of the FOLFOX regimen without any cardiac arrhythmia.

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Acute Peripheral Motor Neuropathy Induced by Oxaliplatin-Correlated Hypokalaemia

Cited by 3 publications

References 27 publications

The roles of ROS and P21 in apoptosis-inducing effect of cepharanthine in human colorectal cancer cells

The roles of ROS and P21 in apoptosis-inducing effect of cepharanthine in human colorectal cancer cells

Capecitabine/glucose/oxaliplatin

FOLFOX regimen induced severe hypokalaemia with hypocalcaemia and hypomagnesaemia

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