Anti-Tumor Effects of Paeoniflorin on Epithelial-To-Mesenchymal Transition in Human Colorectal Cancer Cells

Zhang, Jiawei; Li, Lixin; Wu, Wei‐Zhong; Pan, Ting-Jia; Yang, Zhaoshuo; Yang, Ye

doi:10.12659/msm.912227

Cited by 28 publications

(18 citation statements)

References 25 publications

(22 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Another study shows that Paeoniflorin inhibits the metastasis and invasion of colorectal cancer cells as well as reverses the EMT process by inhibiting the expression of histone deacetylase 2 (HDAC2) in‐vitro experiment, and then affecting the expressions of e‐cadherin and vimentin at the cell level. This experiment has been verified by the tumour xenotransplantation model in vivo and further demonstrates the feasibility of Paeoniflorin in the treatment of colorectal cancer. In 2013, Huang et al .…”

Section: Anticancer Activities Of Paeoniflorin and Its Potential Mechsupporting

confidence: 55%

Paeoniflorin: a monoterpene glycoside from plants of Paeoniaceae family with diverse anticancer activities

Xiang

Zhang

Wei

et al. 2019

Journal of Pharmacy and Pharmacology

View full text Add to dashboard Cite

Objectives Paeoniflorin, a representative pinane monoterpene glycoside in plants of Paeoniaceae family, possesses promising anticancer activities on diverse tumours. This paper summarized the advance of Paeoniflorin on cancers in vivo and in vitro, discussed the related molecular mechanisms, as well as suggested some perspectives of the future investigations. Key findings Anticancer activities of paeoniflorin have been comprehensively investigated, including liver cancer, gastric cancer, breast cancer, lung cancer, pancreatic cancer, colorectal cancer, glioma, bladder cancer and leukaemia. Furthermore, the potential molecular mechanisms corresponding to the antitumour effects of Paeoniflorin might be related to the following aspects: inhibition of tumour cell proliferation and neovascularization, induction apoptosis, and inhibition of tumour invasion and metastasis. Summary Paeoniflorin has wide spectrum antitumour activities; however, in vivo and clinical investigations on antitumour effect of Paeoniflorin are lacking which should be focused on further studies. Our present review on antitumour effects of Paeoniflorin would be beneficial for the further molecular mechanisms study, candidate antitumour drug development and clinical research of Paeoniflorin in the future.

show abstract

Section: Anticancer Activities Of Paeoniflorin and Its Potential Mechsupporting

confidence: 55%

Paeoniflorin: a monoterpene glycoside from plants of Paeoniaceae family with diverse anticancer activities

Xiang

Zhang

Wei

et al. 2019

Journal of Pharmacy and Pharmacology

View full text Add to dashboard Cite

show abstract

“…Paeoniflorin from Paeonia lactiflora has anti-inflammatory effects [231,232]. Paeoniflorin (5-10 µM) can suppress EMT of human colorectal cancer cells and glioblastoma cells and prevent hypoxia-induced EMT of human breast cancer cells [233,234].…”

Section: Reversal Of Emt By Anti-inflammatory Natural Compoundsmentioning

confidence: 99%

Reversal of Epithelial–Mesenchymal Transition by Natural Anti-Inflammatory and Pro-Resolving Lipids

Lee

2019

Cancers

View full text Add to dashboard Cite

Epithelial mesenchymal transition (EMT) is a key process in the progression of malignant cancer. Therefore, blocking the EMT can be a critical fast track for the development of anticancer drugs. In this paper, we update recent research output of EMT and we explore suppression of EMT by natural anti-inflammatory compounds and pro-resolving lipids.A typical signaling pathway of EMT is the transforming growth factor-β1 (TGF-β1) pathway. TGF-β1 induces EMT via SMAD-dependent or non-SMAD signaling pathway [7]. Growth factors including FGF, HGF, IGF1, EGF, and PDGF via receptor tyrosine kinase can induce EMT via signaling pathway of PI3K-AKT and ERK MAPK [8][9][10][11]. Wnt signaling, hedgehog signaling, Notch signaling, hypoxia, and inflammatory tumor microenvironment also involves in EMT [5]. Recently, it has been shown that hippo signaling is also involved in EMT [12]. YAP and TAZ can enhance EMT through upregulation of EMT transcription factors such as forkhead box C2 (FOXC2), snail family zinc finger 1/2 (SNAIL1, SLUG), twist-related protein 1 (TWIST1), and ZEB1 [12-15]. Transcription Factors Involved in EMTNovel players are newly recognized as regulatory transcription factor in the EMT. Brachyury, the T-box transcription factor, is a novel transcription factor implicated in the EMT of cancer cells [16]. Brachyury is known as the target gene of WNT, one of the m ajor signaling pathways of EMT [17]. Foxq1, one of forkhead transcription factor, has also regarded as a novel transcription factor mediating the EMT of gastric cancer [6,18]. Runt-related transcription factor 2 (Runx2) belongs to the runt-related transcription factor family [19]. Runx2 plays a key role in EMT of hepatocellular carcinoma (HCC) [20]. GATA transcription factors are also implicated in the EMT of cancer cells [21].A typical signaling pathway of EMT is the transforming growth factor-β1 (TGF-β1) pathway. TGF-β1 induces EMT via SMAD-dependent or non-SMAD signaling pathway [7]. Growth factors including FGF, HGF, IGF1, EGF, and PDGF via receptor tyrosine kinase can induce EMT via signaling pathway of PI3K-AKT and ERK MAPK [8][9][10][11]. Wnt signaling, hedgehog signaling, Notch signaling, hypoxia, and inflammatory tumor microenvironment also involves in EMT [5]. Recently, it has been shown that hippo signaling is also involved in EMT [12]. YAP and TAZ can enhance EMT through upregulation of EMT transcription factors such as forkhead box C2 (FOXC2), snail family zinc finger 1/2 (SNAIL1, SLUG), twist-related protein 1 (TWIST1), and ZEB1 [12-15]. Transcription Factors Involved in EMTNovel players are newly recognized as regulatory transcription factor in the EMT. Brachyury, the T-box transcription factor, is a novel transcription factor implicated in the EMT of cancer cells [16]. Brachyury is known as the target gene of WNT, one of the major signaling pathways of EMT [17]. Foxq1, one of forkhead transcription factor, has also regarded as a novel transcription factor mediating the EMT of gastric cancer [6,18]. Runt-related transcription factor 2 (Runx2...

show abstract

“…However, this procedure can only assess the survival and proliferation of cancer cells in hepatic tissue. Implantation by injection into the spleen is reportedly one of the ways to establish hepatic metastasis xenograft models (29)(30)(31). There have been several reports of successful establishment of hepatic metastasis models by subcapsular injection of murine cancer cell lines to the spleen (32-34).…”

Section: Peritoneal Metastasis Formation In Nude Mice After Intraperimentioning

confidence: 99%

Establishment of Peritoneal and Hepatic Metastasis Mouse Xenograft Models Using Gastric Cancer Cell Lines

Miwa

Kanda

Umeda

et al. 2019

In Vivo

View full text Add to dashboard Cite

Background/Aim: Establishment of mouse xenograft models is necessary for oncological research and depends on the characteristics of the cell lines and the immune system of the host. In this study, we describe the development of mouse xenograft models using human gastric cancer (GC) cell lines. Materials and Methods: MKN1 stably-expressing luciferase (MKN1-Luc), N87, KATO III, MKN45 stably-expressing luciferase (MKN45-Luc), NUGC4, and OCUM-1 human GC cell lines were injected intraperitoneally into mice to establish peritoneal metastasis models. MKN45-Luc were injected into subcutaneously implanted spleen, and MKN1-Luc and MKN45-Luc were injected directly into the portal veins of mice for the establishment of hepatic metastasis models. Results: Peritoneal metastasis was formed after implantation of MKN1-Luc, N87, KATO III, MKN45-Luc, and NUGC4 in nude mice, but not formed in OCUM-1 even in NOD/SCID mice. After intrasplenic injection of MKN45-Luc, we found no hepatic metastasis formation. We identified hepatic metastasis formation after direct injection of MKN45-Luc and MKN1-Luc into the portal veins of NOD/SCID mice. Conclusion: Peritoneal and hepatic metastasis mouse xenograft models were successfully established using several human GC cell lines. Gastric cancer (GC) is the fourth leading cause of cancerrelated death worldwide (1). Perioperative adjuvant therapy has improved prognosis to a certain degree (2-4). However, Materials and Methods Cell lines and cell culture. MKN1 cells stably expressing luciferase (MKN1-Luc), MKN45 cells stably expressing luciferase (MKN45-Luc), NUGC4, and OCUM-1 were obtained from the Japanese Collection of Research Bio Resources Cell Bank (JCRB) (Osaka, Japan). N87 and KATO III cell lines were purchased from the American Type Culture Collection (ATCC; Manassas, VA, USA). Cells were incubated at 37˚C with 5% CO 2 in the recommended medium supplemented with 10% fetal bovine serum. The characteristics of the gastric cancer cell lines are listed in Table I.

show abstract

Anti-Tumor Effects of Paeoniflorin on Epithelial-To-Mesenchymal Transition in Human Colorectal Cancer Cells

Cited by 28 publications

References 25 publications

Paeoniflorin: a monoterpene glycoside from plants of Paeoniaceae family with diverse anticancer activities

Paeoniflorin: a monoterpene glycoside from plants of Paeoniaceae family with diverse anticancer activities

Reversal of Epithelial–Mesenchymal Transition by Natural Anti-Inflammatory and Pro-Resolving Lipids

Establishment of Peritoneal and Hepatic Metastasis Mouse Xenograft Models Using Gastric Cancer Cell Lines

Contact Info

Product

Resources

About