Efficacy and safety of gemcitabine plus capecitabine in the treatment of advanced or metastatic pancreatic cancer: a systematic review and meta-analysis

Xiao, Bo-Ya; Wang, Bi-Cheng; Lin, Guo-He; Li, Pengcheng

doi:10.21037/apm-20-45

Cited by 12 publications

(9 citation statements)

References 49 publications

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“…It is relatively non-cytotoxic in vitro and can inhibit tumor growth by inhibiting cell division and interfering with protein synthesis. However, it may cause adverse reactions such as vomiting and diarrhea [1]. Clinical data show that the incidence rate of severe diarrhea is 20% approximately, and it is easy to cause patient dose dependence [2,3].…”

Section: Introductionmentioning

confidence: 99%

[Retracted] Study on Huangqi Bazhen Decoction on Relieving Chemotherapy Intestinal Mucositis in Capecitabine Gavage Mice

Shi

Chen

Liu

et al. 2022

Contrast Media & Molecular Imaging

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In order to provide evidence for clinical application, the therapeutic effect and mechanism of Huangqi Bazhen decoction on chemotherapeutic intestinal mucositis induced by capecitabine in mice are investigated. In this paper, the mice are divided into different groups and given capecitabine intragastric administration or treatment drugs. Morphological features of intestinal injury, including villus height shortening, crypt destruction, and apoptosis, are reversed. The experimental results show that Huangqi Bazhen decoction can significantly reduce weight loss and diarrhea during capecitabine treatment. It is also found that GSH-Px and T-SOD can be improved while MDA, IL-1β, and TNF-α are reduced significantly.

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Section: Introductionmentioning

confidence: 99%

[Retracted] Study on Huangqi Bazhen Decoction on Relieving Chemotherapy Intestinal Mucositis in Capecitabine Gavage Mice

Shi

Chen

Liu

et al. 2022

Contrast Media & Molecular Imaging

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“…Gemcitabine is currently one of the main chemotherapeutic drugs used to treat PDA. However, its clinical application fails to prolong the survival time of patients with PDA [ 6 ]. Hence, developing novel robust therapeutic strategies to block cancer metastasis or enhance the therapeutic efficacy of gemcitabine is essential to fulfill the unmet needs of patients with PDA.…”

Section: Introductionmentioning

confidence: 99%

The anthelmintic drug niclosamide induces GSK-β-mediated β-catenin degradation to potentiate gemcitabine activity, reduce immune evasion ability and suppress pancreatic cancer progression

et al. 2022

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Niclosamide, a cell-permeable salicylanilide, was approved by the Food and Drug Administration for its anthelmintic efficiency. A growing body of evidence in recent years suggests that niclosamide exhibits potential tumor-suppressive activity. However, the role and molecular mechanism of niclosamide in pancreatic cancer remain unclear. In this study, niclosamide inhibited proliferation of pancreatic cancer cells (PCCs), induced apoptosis via the mitochondrial-mediated pathway, and suppressed cell migration and invasion by antagonizing epithelial-to-mesenchymal transition. Also, niclosamide inhibited tumor growth and metastasis in pancreatic cancer xenograft mouse models. Mechanistically, niclosamide exerted these therapeutic effects via targeting β-catenin. Niclosamide did not reduce β-catenin mRNA expression in PCCs, but significantly downregulated its protein level. Moreover, niclosamide induced β-catenin phosphorylation and protein degradation. Interestingly, niclosamide also induced GSK-3β phosphorylation, which is involved in the ubiquitination degradation of β-catenin. Pharmacological activation of β-catenin by methyl vanillate and β-catenin overexpression abolished the inhibitory effects of niclosamide. Furthermore, niclosamide potentiated the antitumor effect of the chemotherapy drug gemcitabine and reduced the ability of cancer immune evasion by downregulating the expression levels of PD-L1, which is involved in T cell immunity. Thus, our study indicated that niclosamide induces GSK-β-mediated β-catenin degradation to potentiate gemcitabine activity, reduce immune evasion ability, and suppress pancreatic cancer progression. Niclosamide may be a potential therapeutic candidate for pancreatic cancer.

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“…Gemcitabine is currently the first-line drug for PDA chemotherapy, but chemotherapy resistance is widespread and has become the main reason for the failure of PDA chemotherapy [ 29 ]. Therefore, it is crucial to inhibit gemcitabine resistance and promote its anti-PDA efficacy.…”

Section: Resultsmentioning

confidence: 99%

The anti-dysenteric drug fraxetin enhances anti-tumor efficacy of gemcitabine and suppresses pancreatic cancer development by antagonizing STAT3 activation

Guo

Xiao

Guo

et al. 2021

Aging

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Fraxetin, a natural product isolated and purified from the bark of Fraxinus bungeana A.DC. , has anti-inflammatory, analgesic, and anti-dysenteric activities. This study aimed to investigate the anti-tumor effects of fraxetin in pancreatic ductal adenocarcinoma (PDA). The effects of fraxetin on the malignant biological behavior of PDA were evaluated. Besides, the effects of fraxetin on the sensitivity of PCCs to gemcitabine, angiogenesis, the epithelial-mesenchymal transition (EMT), glucose metabolism, reactive oxygen species (ROS), and STAT3 activity were analyzed. By reversing the EMT, fraxetin suppressed proliferation, invasion, and migration, and induced mitochondrial-dependent apoptosis in PCCs. Also, treatment with fraxetin inhibited PDA growth and metastasis in nude mouse models. Furthermore, fraxetin made PCCs more sensitive to the chemotherapy drug gemcitabine. Mechanically, fraxetin treatment suppressed oncogenic KRAS-triggered STAT3 activation in PCCs and PDA tissues. Fraxetin shows significant interactions with STAT3 Src Homology 2 (SH2) domain residues, thereby preventing its homo-dimer formation, which then blocks the activation of downstream signal pathways. The anti-tumor activity of fraxetin in PDA was functionally rescued by a STAT3 activator colivelin. As a result, fraxetin hindered hypoxia-induced angiogenesis by decreasing HIF-1α and VEGFA expression, controlled glucose metabolism by reducing GLUT1 expression, inhibited the EMT by blocking the Slug-E-cadherin axis, and drove ROS-mediated apoptosis by regulating the STAT3-Ref1 axis. In conclusion, fraxetin enhances the anti-tumor activity of gemcitabine and suppresses pancreatic cancer development by antagonizing STAT3 activation.

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Efficacy and safety of gemcitabine plus capecitabine in the treatment of advanced or metastatic pancreatic cancer: a systematic review and meta-analysis

Cited by 12 publications

References 49 publications

[Retracted] Study on Huangqi Bazhen Decoction on Relieving Chemotherapy Intestinal Mucositis in Capecitabine Gavage Mice

[Retracted] Study on Huangqi Bazhen Decoction on Relieving Chemotherapy Intestinal Mucositis in Capecitabine Gavage Mice

The anthelmintic drug niclosamide induces GSK-β-mediated β-catenin degradation to potentiate gemcitabine activity, reduce immune evasion ability and suppress pancreatic cancer progression

The anti-dysenteric drug fraxetin enhances anti-tumor efficacy of gemcitabine and suppresses pancreatic cancer development by antagonizing STAT3 activation

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