Weekly Taxotere and cisplatin with continuous-infusion 5-fluoruracil for the treatment of advanced gastric and esophageal cancer: a prospective, observational, single-institution experience

Piacentini, Paolo; Durante, E; Trolese, Annarita; Mercanti, Anna; Bonetti, Andrea

doi:10.1007/s10120-011-0078-5

Cited by 6 publications

(3 citation statements)

References 20 publications

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“…Cisplatin (DDP) is the frequently-used chemotherapeutic agent shown to improve survival in patients with ESCC, as established by randomized controlled trials and therefore approved by the Food and Drug Administration for this use [45-48]. Resistance to chemotherapy, especially to DDP, has presented itself as a major obstacle in treatment of advanced ESCC.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of DNA damage-induced 45 α gene contributes to esophageal squamous cell cancer by promoter hypomethylation

Wang

Yin

et al. 2012

J Exp Clin Cancer Res

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BackgroundEnvironmental factors-induced dysfunction of esophageal squamous epithelium, including genomic DNA impairment and apoptosis, play an important role in the pathogenesis of esophageal squamous cell cancer. DNA damage-induced 45α (GADD45α) has been found promoting DNA repair and removing methylation marker, Therefore, in this study we will investigate whether GADD45α expression is induced and its mechanism in esophageal squamous cell cancer.MethodsTwo human esophageal squamous cell lines (ESCC), ECA109 and KYSE510 were cultured in RPMI-1640 medium supplemented with 10% fetal bovine serum (FBS). Lipofectamine 2000 was used to transfect cells. mRNA level of GADD45α was measured by reverse transcription-quantitive PCR (RT-qPCR), protein level of GADD45α was detected by western blot and Immunohistochemistry. Global DNA methylation of tissue sample was measured using the Methylamp Global DNA Methylation Quantification Ultra kit (Epigentek Group) and promoter methylation was measured by bisulfite sequencing.ResultsGADD45a mRNA and protein levels were increased significantly in tumor tissue than that in adjacent normal tissue. Hypomethylation of global genomic DNA and GADD45α promoter were found in ESCC. The cell sensitivity to Cisplatin DDP was decreased significantly in Eca109 and Kyse510 cells, in which GADD45α expression was down-regulated by RNA interference (RNAi). In addition, silence of GADD45a expression in ESCC cells inhibited proliferation and promoted apoptosis.ConclusionOverexpression of GADD45α gene is due to DNA hypomethylation in ESCC. GADD45α may be a protective factor in DDP chemotherapy for esophageal squamous cell carcinoma.

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Section: Discussionmentioning

confidence: 99%

Overexpression of DNA damage-induced 45 α gene contributes to esophageal squamous cell cancer by promoter hypomethylation

Wang

Yin

et al. 2012

J Exp Clin Cancer Res

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“…The study reported here showed that ILK silencing could reverse the drug resistance of SGC7901/ DDP, a human gastric carcinoma cell lines with multi-drug resistance. A panel of molecules associated with multiple drug resistance and tumorigenicity were solidly regulated Cisplatin is a major chemotherapy drug in gastric carcinoma treatment (Piacentini et al, 2012). Drug resistance is a common problem faced in gastric carcinoma care and therefore new treatment strategies are in urgent.…”

Section: Discussionmentioning

confidence: 99%

Role of Integrin-Linked Kinase in Multi-drug Resistance of Human Gastric Carcinoma SGC7901/DDP Cells

Song

Jiang²,

Zhao³

2012

Asian Pacific Journal of Cancer Prevention

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Gastric carcinoma is a leading cause of cancer death in the world and multi-drug resistance (MDR) is an essential aspect of gastric carcinoma chemotherapy failure. Recent studies have shown that integrin-linked kinase (ILK) is involved in metastasis of human tumors, expression silencing of ILK inhibiting the metastasis of several types of cultured human cancer cells. However, the role and potential mechanism of ILK to reverse the multidrug resistance in human gastric carcinoma is not fully clear. In this report, we focused on roles of expression silencing of ILK in multi-drug resistance reversal of human gastric carcinoma SGC7901/DDP cells, including increased drug sensitivity to cisplatin, cell apoptosis rates, and intracellular accumulation of Rhodamine-123, and decreased mRNA and protein expression of multi-drug resistance gene (MDR1), multi-drug resistanceassociated protein (MRP1), excision repair cross-complementing gene 1 (ERCC1), glutathione S-transferase -π (GST-π) and RhoE, and transcriptional activation of AP-1 and NF-κB in ILK silenced SGC7901/DDP cells. We also found that there was a decreased level of p-Akt and p-ERK. The results indicated that ILK might be used as a potential therapeutic strategy to combat multi-drug resistance through blocking PI3K-Akt and MAPK-ERK pathways in human gastric carcinoma.

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“…To explore the effect and mechanism of ANXA2 on MDR in GC, we successfully established a DDP resistant cell line SGC7901/DDP after continual exposure of SGC7901 to cisplatin, a major chemotherapy drug in gastric carcinoma treatment [30].The results showed that the resistance index was 23.4. The establishment of SGC7901/DDP cells has provided a powerful tool for further study of the effect and mechanism of ANXA2 on MDR.…”

Section: Discussionmentioning

confidence: 99%

Annexin A2 is implicated in multi-drug-resistance in gastric cancer through p38MAPK and AKT pathway

Zhang¹,

Li²,

Fan³

et al. 2014

neo

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Studies have shown that Annexin A2 (ANXA2) is related with tumor proliferation, apoptosis, differentiation, invasion, migration, and drug resistance. The purpose of this study was to investigate the role and its mechanisms of ANXA2 in multidrug-resistance (MDR) in gastric cancer. ANXA2 expression in both gastric cancer tissues and cell lines were detected by quantitative real-time PCR (RT-qPCR) and Western blotting. The cell proliferation was measured by SRB assay. The pool of siRNA against ANXA2 was designed and synthesized and then transfected into resistant gastric cancer SGC7901/DDP cells. ANXA2 expression was detected by RT-qPCR and Western blotting. Drug sensitivities of SGC7901/DDP cells to P-gp-related drug (doxorubicin) and P-gp-non-related drugs (5-FU and cisplatin) were measured by SRB assay.Expression of MDR-related genes and phosphorylation of AKT and MAPKs were also detected by RT-qPCR and Western blotting. Results showed that ANXA2 expression was significantly higher in gastric specimens than that in normal tissues, and negatively correlated with the differentiation level of gastric cancer. In addition, ANXA2 expression level was higher in SGC7901/DDP cells than that in parent SGC7901 cells. After knock-down ANXA2 expression using ANXA2 small interfering RNA, the drug sensitivity of SGC7901/DDP cells to doxorubicin, 5-FU and DDP increased. Delivery of ANXA2 siRNA significantly downregulated the expression of P-gp, MRP1 and Bcl-2, while markedly upregulated Bax in SGC7901/DDP cells. However, several other MDR factors such as GST-π, TOPO-I and TOPO-II had no obvious changes. Additionally, phosphorylation of P38MAPK and AKT, but not ERK1/2 or JNKs was specifically decreased in SGC7901/DDP cells after ANXA2 siRNA delivery. Importantly, P38MAPK and AKT inhibitor increased the drug sensitivity of SGC701/DDP cells in a similar way as ANXA2 siRNAs does. ANXA2 is involved in gastric cancer MDR through regulating p38MAPK and AKT pathways as well as certain MDR factors.

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Weekly Taxotere and cisplatin with continuous-infusion 5-fluoruracil for the treatment of advanced gastric and esophageal cancer: a prospective, observational, single-institution experience

Cited by 6 publications

References 20 publications

Overexpression of DNA damage-induced 45 α gene contributes to esophageal squamous cell cancer by promoter hypomethylation

Overexpression of DNA damage-induced 45 α gene contributes to esophageal squamous cell cancer by promoter hypomethylation

Role of Integrin-Linked Kinase in Multi-drug Resistance of Human Gastric Carcinoma SGC7901/DDP Cells

Annexin A2 is implicated in multi-drug-resistance in gastric cancer through p38MAPK and AKT pathway

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