Albendazole suppresses cell proliferation and migration and induces apoptosis in human pancreatic cancer cells

The receptor for advanced glycation end products (RAGE) contributes to many cellular aspects of pancreatic cancer including cell proliferation, migration, and survival. Studies have shown that RAGE activation by its ligands promotes pancreatic tumor growth by stimulating both cell proliferation and migration. In this study, we investigated the effect of RAGE up-regulation on the proliferation and migration of the human pancreatic cancer Panc-1 cell-line. We show that moderate overexpression of RAGE in Panc-1 cells results in increased cell proliferation, but decreased cell migration. The observed cellular changes were confirmed to be RAGE-specific and reversible by using RAGE-specific siRNAs and the small molecule RAGE inhibitor FPS-ZM1. At the molecular level, we show that RAGE up-regulation was associated with decreased activity of FAK, Akt, Erk1/2, and NF-κB signaling pathways and greatly reduced levels of α2 and β1 integrin expression, which is in agreement with the observed decreases in cell migration. We also demonstrate that RAGE up-regulation changes the expression of key molecular markers of epithelial-to-mesenchymal transition (EMT). Our results suggest that in the absence of stimulation by external ligands, RAGE up-regulation can differently modulate cell proliferation and migration in pancreatic cancer cells and regulates partly EMT.

Download Full-text

Long Noncoding RNA PVT1 Promotes EMT and Cell Proliferation and Migration Through Downregulating p21 in Pancreatic Cancer Cells

Technology in Cancer Research & Treatment ◽

10.1177/1533034617700559 ◽

2017 ◽

Vol 16 (6) ◽

pp. 819-827 ◽

Cited By ~ 31

Author(s):

Bao-Qiang Wu ◽

Yong Jiang ◽

Feng Zhu ◽

Dong-Lin Sun ◽

Xiao-Zhou He

Keyword(s):

Pancreatic Cancer ◽

Cell Proliferation ◽

Cancer Cells ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Pancreatic Cancer Cells ◽

Cell Proliferation And Migration ◽

And Migration ◽

Proliferation And Migration

Download Full-text

Long non-coding RNA FAM83H-AS1 induced by adipose-derived stem cells promotes breast and pancreatic cancer cell proliferation and migration

10.21203/rs.3.rs-23457/v1 ◽

2020 ◽

Cited By ~ 1

Author(s):

Jianing Tang ◽

Qiuxia Cui ◽

Dan Zhang ◽

Xing Liao ◽

Yan Gong ◽

...

Keyword(s):

Pancreatic Cancer ◽

Stem Cells ◽

Cell Proliferation ◽

Adipose Derived Stem Cells ◽

Unfolded Protein ◽

Pancreatic Cancer Cells ◽

Cell Proliferation And Migration ◽

And Migration ◽

Protein Response ◽

Proliferation And Migration

Abstract Background Stromal cells recruited to the tumor microenvironment and long non-coding RNAs (lncRNAs) in the tumor cells regulate cancer progression. However, their relationship is largely unknown. Methods In the current study, we identified the effects of lncRNA FAM83H-AS1, induced by adipose-derived stem cells (ADSCs) during tumor development, and explored the underlying mechanisms using a coculture cell model. Adipose tissues were obtained from healthy female donors, the expression of stromal markers on cell surface of expanded ADSCs were confirmed using immunofluorescence analysis. The breast and pancreatic cancer cells were cultured with or without ADSCs using 24-well transwell chamber systems with 8.0 µm pore size. Results Our results showed that FAM83H-AS1 was upregulated in breast and pancreatic cancers and associated with poor prognosis. ADSCs further induced FAM83H-AS1 and increased tumor cell proliferation via promoting G1/S transition through cyclin D1, CDK4 and CDK6. Wound healing, modified Boyden chamber and immunoblotting assays demonstrated that ADSCs induced epithelial-mesenchymal transition and migration of breast and pancreatic cancer cells in a FAM83H-AS1-dependent manner. And ADSC-induced FAM83H-AS1 increased unfolded protein response through AKT/XBP1 pathway. Conclusion In conclusion, our results indicated that ADSCs promoted breast and pancreatic cancer development via inducing cell proliferation and migration, as well as unfolded protein response through FAM83H-AS1.

Download Full-text

SIRT1 promotes the proliferation and metastasis of human pancreatic cancer cells

Tumor Biology ◽

10.1177/1010428317691180 ◽

2017 ◽

Vol 39 (3) ◽

pp. 101042831769118 ◽

Cited By ~ 11

Author(s):

Jianguang Jin ◽

Zhijie Chu ◽

Pengfei Ma ◽

Yuanpu Meng ◽

Yanhui Yang

Keyword(s):

Pancreatic Cancer ◽

Cell Proliferation ◽

Cancer Cell ◽

Cancer Cell Proliferation ◽

Pancreatic Cancer Cells ◽

Cell Proliferation And Migration ◽

Proliferation And Metastasis ◽

And Migration ◽

Cancer Tissues ◽

Proliferation And Migration

SIRT1 plays an important role in human malignant progression, inducing cancer cell proliferation and metastasis by regulating downstream gene expressions. However, little is known about the underlying mechanisms in which SIRT1 promotes pancreatic cancer tumorigenesis. The aim of this study is to investigate the SIRT1 expression levels and biological functions in promoting pancreatic cancer progression. We first investigated the expression of SIRT1 in a series of pancreatic cancer tissues as well as in a panel of pancreatic cancer cell lines. The effect of SIRT1 on cell activity was explored by knockdown experiments. Cell growth was measured using the MTT assay and colony-formation assay. Migration and invasion were tested using transwell assay. Our results showed that the expression of SIRT1 was significantly up-regulated both in pancreatic cancer tissues and cell lines. Knockdown of SIRT1 suppressed cell proliferation and migration of pancreatic cancer cells. This is the first report to disclose the role of SIRT1 in regulation of pancreatic cancer cell proliferation and migration, which may provide a potential therapeutic target for pancreatic cancer patients.

Download Full-text

The Role of the Novel Selective Dual Inhibitor of the Igf-Ir/Ir on Proliferation and Migration of Human Pancreatic Cancer Cells

Annals of Oncology ◽

10.1093/annonc/mdt203.43 ◽

2013 ◽

Vol 24 ◽

pp. iv49

Author(s):

Stephanie Booy ◽

Casper Van Eijck ◽

Peter Van Koetsveld ◽

Fadime Dogan ◽

Joop Janssen ◽

...

Keyword(s):

Pancreatic Cancer ◽

Cancer Cells ◽

Human Pancreatic Cancer ◽

The Novel ◽

Dual Inhibitor ◽

Pancreatic Cancer Cells ◽

And Migration ◽

Proliferation And Migration

Download Full-text

Deguelin inhibits proliferation and migration of human pancreatic cancer cells in vitro targeting hedgehog pathway

Oncology Letters ◽

10.3892/ol.2016.4928 ◽

2016 ◽

Vol 12 (4) ◽

pp. 2761-2765 ◽

Cited By ~ 16

Author(s):

Wen Zheng ◽

Shiliu Lu ◽

Haolei Cai ◽

Muxing Kang ◽

Wenjie Qin ◽

...

Keyword(s):

Pancreatic Cancer ◽

Cancer Cells ◽

Hedgehog Pathway ◽

Human Pancreatic Cancer ◽

Pancreatic Cancer Cells ◽

And Migration ◽

Proliferation And Migration

Download Full-text

Effect of miR-210 on Proliferation and Migration of Pancreatic Cancer Cells Through Regulating Runx3 Level

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2020.2519 ◽

2020 ◽

Vol 10 (12) ◽

pp. 1827-1831

Author(s):

Wanggang Xu ◽

Yingmin Kuang ◽

Dan Wang ◽

Zhen Li ◽

Renpin Xia

Keyword(s):

Pancreatic Cancer ◽

Cell Proliferation ◽

Cell Migration ◽

Cancer Cells ◽

Suppressor Gene ◽

Cancer Tissue ◽

Pancreatic Cancer Cells ◽

And Migration ◽

Pcr Targeting ◽

Proliferation And Migration

miR-210 is closely related to the occurrence of pancreatic cancer. In addition, Runx3 is a tumor suppressor gene and inhibits tumorigenesis. However, miR-210?s effect on Runx3 level is unclear. Therefore, Our study explored miR-210?s effect on the proliferation and migration of pancreatic cancer cells. PANC-1 cell line was transfected with miR-210 Mimics or miR-210 Mimic+pFBD-Runx3 plasmids followed by analysis of miR-210 and Runx3 level by qRT-PCR, targeting relationship by the dual fluorescein reporter assay, Runx3 and Tubulin protein expression by Western blot, cell proliferation by MTT assay and cell migration by Transwell assay. Compared with normal tissue, miR-210 was significantly upregulated in pancreatic cancer tissue (P < 0.01), while Runx3 mRNA was significantly downregulated (P < 0.01). Runx3 was a target protein of miR-210. miR-210 Mimics transfection significantly reduced Runx3 level and increased cell proliferation, which was significantly reduced in the miR-210 Mimic+pFBD-Runx3 group. miR-210 Mimics significantly promote cell migration and the addition of Runx3 prevented miR-210 Mimics-induced cell migration. miR-210 binds to the 3′-UTR region of Runx3 mRNA, reduces Runx3 expression, and promotes cell proliferation and migration. Increased Runx3 can inhibit miR-210?s effect on pancreatic cancer cells.

Download Full-text