Increased p38-MAPK is responsible for chemotherapy resistance in human gastric cancer cells

Guo, Xianling; Ma, Ning; Wang, Jin; Song, Jianrui; Bu, Xinxin; Cheng, Yue; Sun, Kai; Xiong, Hu; Jiang, Guocheng; Zhang, Baihe; Wu, Mengchao; Wei, Lixin

doi:10.1186/1471-2407-8-375

Cited by 122 publications

(94 citation statements)

References 45 publications

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“…It has also been reported that NF-κB levels are significantly associated with poor prognosis of gastric cancer (27). Guo et al revealed that the activation of the NF-κB dimer was significantly higher in drug-resistant gastric cancer cell lines than its parental cell lines (28). Therefore, NF-κB is proposed as a specific molecule related to drug resistance and is a potential therapeutic target for the treatment strategy of gastric carcinoma.…”

Section: Discussionmentioning

confidence: 99%

Paeoniflorin modulates multidrug resistance of a human gastric cancer cell line via the inhibition of NF-κB activation

Liu

2011

Mol Med Report

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Abstract.Research into the evasion of drug resistance and adverse effects is highly significant and urgent in the clinic. Therefore, accumulating studies have focused on the development of novel target-specific molecules related to drug resistance, and the establishment of rational therapeutic approaches. Currently, studies have shown that NF-κB activation may play an essential role in the development of chemotherapy resistance in carcinoma cells. Paeoniflorin, a principal bioactive component of the root of Paeonia lactiflora Pall., has been reported to exhibit various pharmacological effects. In the present study, we reported for the first time that paeoniflorin at non-toxic concentrations may effectively modulate multidrug resistance (MDR) of the human gastric cancer cell line SGC7901/vincristine (VCR) via the inhibition of NF-κB activation and, at least partly, by subsequently downregulating its target genes MDR1,

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Section: Discussionmentioning

confidence: 99%

Paeoniflorin modulates multidrug resistance of a human gastric cancer cell line via the inhibition of NF-κB activation

Liu

2011

Mol Med Report

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“…It was demonstrated that the active form of PI3K is related to an increase of Pgp expression (46). Furthermore, several molecular pathways, such as NF-κB, ERK/MAPK, and p38-MAPK, among others, are also associated with the regulation of Pgp expression in cancer cells (47)(48)(49). A recent study showed that the MDR phenotype in K562 cells could be reversed by inhibition of the NF-κB pathway, suggesting a regulation of Pgp through modulation of NF-κB (50).…”

Section: Discussionmentioning

confidence: 99%

P-glycoprotein and survivin simultaneously regulate vincristine-induced apoptosis in chronic myeloid leukemia cells

Souza

Vasconcelos²,

Reis³

et al. 2011

Int J Oncol

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Abstract. Overexpression of P-glycoprotein (Pgp/ABCB1) in tumor cells is associated with a classic phenotype of multidrug resistance (MDR). Moreover, some members of the inhibitor of apoptosis protein (IAP) family, such as survivin, contribute to an apoptosis-resistant phenotype, by inhibiting chemotherapyinduced cell death and promoting MDR. By using Western blotting, qRT-PCR, Annexin V and immunofluorescence assays we have demonstrated a relationship between Pgp and survivin in a prior sensitive chronic myeloid leukemia (CML) cell line (K562). A high dose of vincristine induced a concomitant overexpression of Pgp and survivin, which was associated with a low apoptotic index in the K562 cell line. In addition, we observed a cytoplasmic co-localization of Pgp and survivin, suggesting a functional association between these two proteins in apoptosis control by a common mechanism. In summary, our data suggest that Pgp and survivin should be analyzed in aggregate because they may have significant impact on drug resistance in CML cells.

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“…it can be stimulated by various stresses such as uv and γ irradiation, osmotic stress, heat shock and some chemotherapeutic drugs (19). a recent study (20) found that inhibition of p38 MaPK downregulated a multidrug-resistance i gene, which was believed to be responsible for chemotherapy resistance in gastric cancer cells. However, to date we could not find any report providing insight into the details of the role of p38 MaPK pathway in 5-fu resistance in crc cells.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of the p38 MAPK pathway sensitises human colon cancer cells to 5-fluorouracil treatment

Shi

2011

Int J Oncol

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Abstract. colorectal cancer is the third most common cause of cancer-related deaths in the Western world. 5-fluorouracil (5-fu) based chemotherapeutic regimes have been the mainstay of systemic treatment for disseminated colorectal cancer for many years. However, it only produces a 25% response rate due to the drug-resistance. the mitogen-activated protein kinase (MaPK) pathway is involved in the anti-apoptotic process; its activation provides cancer cells with a survival advantage to escape the apoptotic challenge. this study assessed whether the p38 MaPK pathway is involved in 5-fu resistance in colorectal cancer cells. 5-fu only or 5-fu combined with a p38 MaPK pathway inhibitor (SB203580) was used to treat 5-fu-resistant colorectal cancer cells. the effect of the treatment on cell viability, death and caspase activities was assessed. Western blotting was used to investigate the responses of apoptosis-related proteins following the treatment. results showed that p38 MaPK inhibitor significantly increased colorectal cancer cell sensitivity to 5-fu. SB203580 in combination with 5-FU significantly reduced cell viability (P<0.01), and increased cell death and cellular caspase activity (P<0.01). Western blotting data revealed that SB203580 sensitises cancer cells to 5-fu due to an increase in Bax expression. these findings suggest that p38 MAPK is involved in cancer cell survival, and that the inhibition of p38 MaPK can enhance 5-fu to kill colorectal cancer cells.

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Increased p38-MAPK is responsible for chemotherapy resistance in human gastric cancer cells

Cited by 122 publications

References 45 publications

Paeoniflorin modulates multidrug resistance of a human gastric cancer cell line via the inhibition of NF-κB activation

Paeoniflorin modulates multidrug resistance of a human gastric cancer cell line via the inhibition of NF-κB activation

P-glycoprotein and survivin simultaneously regulate vincristine-induced apoptosis in chronic myeloid leukemia cells

Inhibition of the p38 MAPK pathway sensitises human colon cancer cells to 5-fluorouracil treatment

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