A polymeric prodrug of cisplatin based on pullulan for the targeted therapy against hepatocellular carcinoma

Wang, Yan; Liu, Yuanyuan; Liu, Yang; Zhou, Wen; Wang, Hemei; Wan, Guoyun; Sun, Duxin; Zhang, Ning; Wang, Yinsong

doi:10.1016/j.ijpharm.2015.02.027

Cited by 39 publications

(20 citation statements)

References 35 publications

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“…Extensive efforts have been devoted to evaluation of different cytotoxic agents by different methods, including Metronomic capecitabine [146], gemcitabine [147], cisplatin [148] and doxorubicin [149], for treatment of advanced HCC. But the objective response rate (ORR) to a single cytotoxic regimen was merely 0-10% with no significant survival benefit [150].…”

Section: Combination Of Cytotoxic Chemotherapeutic Agentssupporting

confidence: 67%

Potential molecular, cellular and microenvironmental mechanism of sorafenib resistance in hepatocellular carcinoma

et al. 2015

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Section: Combination Of Cytotoxic Chemotherapeutic Agentssupporting

confidence: 67%

Potential molecular, cellular and microenvironmental mechanism of sorafenib resistance in hepatocellular carcinoma

et al. 2015

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“…Cisplatin, the first generation of platinum drugs, is one of the most active anticancer chemotherapeutic drugs (3). As a cell cycle non-specific drug, it can inhibit effectively the proliferation of HCC by the cytotoxic effect (4,5). The main targets of cisplatin are DNA, RNA and proteins with strong affinity to the nucleus (6).…”

Section: Introductionmentioning

confidence: 99%

Cisplatin induces HepG2 cell cycle arrest through targeting specific long noncoding RNAs and the p53 signaling pathway

et al. 2016

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Cisplatin has been used effectively in the treatment of hepatocellular carcinoma (HCC). Long noncoding RNAs (lncRNAs) were recently reported to contribute to the pathogenesis and progression of HCC. Their molecular mechanism related to cisplatin treatment remains unclear. The purpose of this study is to identify specific lncRNAs and to clarify their functions in HCC after cisplatin exposure. Reannotation and identification of differentially expressed lncRNAs were performed using the microarray data set GSE38122 in the Gene Expression Omnibus database. Four significantly differentially expressed lncRNAs (RP11-134G8.8, RP11-612B6.2, RP11-363E7.4 and RP1-193H18.2) were identified in HepG2 cells exposed to cisplatin by bioinformatics methods. The upregulated RP11-134G8.8 and RP11-363E7.4 and the downregulated RP1-193H18.2 were confirmed by reverse transcription-quantitative polymerase chain reaction. Furthermore, 57 significant co-expressing genes and their corresponding pathways were annotated and identified. The p53 signaling pathway showed the most significant difference among all pathways. Based on these results, the cell cycle and three key genes, cyclin-dependent kinase inhibitor 1A (CDKN1A, also known as p21), tumor protein p53 inducible protein 3 (TP53I3) and wild-type p53-induced phosphatase 1 (Wip1, also known as PPM1D), were examined. CDKN1A, TP53I3 and PPM1D were all downregulated by RP1-193H18.2 but upregulated by RP11-134G8.8 and RP11-363E7.4. And obvious S phase arrest was induced by cisplatin treatment for 24 h in HepG2 cells. Finally, the immunofluorescence results showed upregulation of TP53I3 and Wip1 and downregulation of p21 at the protein level. The results suggested that the lncRNAs RP11-134G8.8, RP11-363E7.4 and RP1-193H18.2, and their co-expression genes, which annotated into the p53 signaling pathway, could be potential targets for cisplatin treatment.

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“…Moreover, rapid establishment of the peripheral collateral blood supply provides sufficient nutrition for the remaining tumor tissue and thereby induces proliferation [12]. Multiple intratumor injections of cisplatin can not only kill microcarcinoma lesions in tumors and vessels, but can also kill tumor cells that moved into the surrounding area; this can continue to kill tumor cells surviving from lipiodol and make for a better prognosis [13]. In this paper, more cases with PR/CR and fewer cases with NC/PD were found in the TACE/cisplatin group; Blood FAP also significantly declined in the TACE/cisplatin group.…”

Section: Discussionmentioning

confidence: 99%

Assessment of the feasibility of TACE combined with intratumoral injection of cisplatin in hepatocellular carcinoma

et al. 2015

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The feasibility of transcatheter arterial chemo-embolization (TACE) combined with intratumoral injection of cisplatin as treatment for hepatocellular carcinoma. 30 cases receiving TACE were denoted the TACE group, another 30 cases receiving TACE combined with an intratumoral multi-point injection of cisplatin were denoted the TACE/cisplatin group. Cases with partial remission/complete remission (PR/CR) were analyzed using 2 tests; alpha fetoprotein (AFP), aspartate amino transferase (AST), total bilirubin (TBIL), erythrocyte, and platelet levels were detected and the differences between two groups were analyzed using the Student’s t-test; cases with complications, including intrahepatic metastasis (IM), upper gastrointestinal bleeding (UGB), and liver failure were also counted. The correlation of clinical parameters with PR/CR was analyzed using multifactorial correlation analysis. Cases with PR/CR in the TACE/cisplatin group were significantly more than in TACE group, accompanied by significant declination in FAP. There were no significant differences of AST, ALT, TBIL, blood urea nitrogen (BUN), white blood cells (WBC), red blood cells (RBC), and platelets (PLT) between two groups; 3 cases with IM, one case with UGB and one case with LF were found in the TACE group, but only 1 case with IM was found in the TACE/cisplatin group. In addition, tumor stage was correlated with PR/CR. We concluded that TACE combined with intratumoral injection of cisplatin was more effective than TACE, and with fewer complications and side effects.

show abstract

A polymeric prodrug of cisplatin based on pullulan for the targeted therapy against hepatocellular carcinoma

Cited by 39 publications

References 35 publications

Potential molecular, cellular and microenvironmental mechanism of sorafenib resistance in hepatocellular carcinoma

Potential molecular, cellular and microenvironmental mechanism of sorafenib resistance in hepatocellular carcinoma

Cisplatin induces HepG2 cell cycle arrest through targeting specific long noncoding RNAs and the p53 signaling pathway

Assessment of the feasibility of TACE combined with intratumoral injection of cisplatin in hepatocellular carcinoma

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