ZFX Promotes Proliferation and Metastasis of Pancreatic Cancer Cells via the MAPK Pathway

Song, Xiaoling; Zhu, Minghui; Zhang, Fahong; Zhang, Fei; Zhang, Yijian; Hu, Yunping; Jiang, Lin; Hao, Yajuan; Chen, Shili; Zhu, Qin; Huang, Wen; Lu, Jianhua; Gu, Jun; Gong, Wei; Li, Maolan; Liu, Yingbin

doi:10.1159/000491727

Cited by 19 publications

(14 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The mammalian cell cycle is controlled by a series of highly regulated processes, and its dysregulation is a hallmark of human cancer19-21. Progression through the cell cycle depends on the activation of cyclin-dependent kinases (CDKs) and their regulatory subunits, the cyclins22. In the present study, we found that treatment with liensinine could induce gastric cancer cells to arrest at the G0/G1 phase.…”

Section: Discussionmentioning

confidence: 56%

Liensinine inhibited gastric cancer cell growth through ROS generation and the PI3K/AKT pathway

Yang¹,

Yu²,

Si³

et al. 2019

J. Cancer

View full text Add to dashboard Cite

Liensinine, an isoquinoline alkaloid extracted from the seed embryo of Nelumbo nucifera Gaertn, has been shown to exhibit various phrenological effects, including anti‑cancer activity. The aim of this study is to investigate the effects and mechanisms of liensinine in human gastric cancer cells. In this study, we found liensinine can significantly inhibit gastric cancer cell proliferation in vitro and in vivo. Liensinine inducedgastric cancer cell apoptosis by increasing cleaved PARP, caspased 3 and caspased 9. Moreover, liensinine induced cycle arrest by downregulatingcyclinD1/cyclin‑dependent kinase4 and phosphorylated protein kinase B. Furthermore, we found liensinine increases ROS levels and inhibits the PI3K/AKT pathway. These data suggested that liensinine might represent a novel and effective agent against gastric cancer.

show abstract

Section: Discussionmentioning

confidence: 56%

Liensinine inhibited gastric cancer cell growth through ROS generation and the PI3K/AKT pathway

Yang¹,

Yu²,

Si³

et al. 2019

J. Cancer

View full text Add to dashboard Cite

show abstract

“…Our findings indicate that miR-218 suppresses TNBC progression by negatively regulating the zinc finger transcription factor ZFX. ZFX has been implicated in various cancers including pancreatic [50], gastric [51], hepatocellular carcinoma [52], malignant glioma [53], and gallbladder cancer [54]. Silencing ZFX suppressed breast cancer cell proliferation [55].…”

Section: Discussionmentioning

confidence: 99%

CCAT1 promotes triple-negative breast cancer progression by suppressing miR-218/ZFX signaling

Han

Fan

et al. 2019

Aging

View full text Add to dashboard Cite

Long non-coding RNAs (lncRNAs) regulate cancer development and progression. Here, we investigated the role of the lncRNA CCAT1 in triple-negative breast cancer (TNBC). CCAT1 expression was higher in TNBC cells than normal breast epithelial cells. Additionally, CCAT1 expression was higher in TNBC patient tumor tissue than adjacent normal breast tissue. Silencing CCAT1 inhibited TNBC cell proliferation, migration, and invasion in vitro , and tumor growth and progression in vivo . Bioinformatics analysis revealed that microRNA-218 (miR-218) is a potential target of CCAT1. Silencing CCAT1 resulted in an increase in miR-218 expression and inhibited TNBC cell proliferation, migration, and invasion. Silencing miR-218 reversed the effects of CCAT1 knockdown on cell proliferation, migration, and invasion, suggesting that CCAT1 promotes TNBC progression by downregulating miR-218 expression. We identified the zinc finger protein ZFX as a putative downstream target of miR-218 through bioinformatics analysis. ZFX expression was higher in TNBC than normal breast cell lines and higher in TNBC tumor tissue than adjacent normal breast tissue. Overexpression of ZFX reversed the tumor-suppressive effects of miR-218 on TNBC cell proliferation, migration, and invasion. Our data indicate that CCAT1 promotes TNBC progression by targeting the miR-218/ZFX axis.

show abstract

“…Quantitative real-time PCR was performed to amplify the target genes and measure their expression with glyceraldehyde 3-phosphate dehydrogenase ( GAPDH ) as an internal loading control. The SYBR-Green method was used according to the manufacturer’s instructions for this process and the results were analyzed with the 2 −ΔΔCT method described previously 11…”

Section: Methodsmentioning

confidence: 99%

NETO2 promotes pancreatic cancer cell proliferation, invasion and migration via activation of the STAT3 signaling pathway

Li¹,

Zhang²,

Liu³

2019

CMAR

View full text Add to dashboard Cite

Purpose: The biological functions of neuropilin and tolloid-like 2 ( NETO2 ) in the progression of pancreatic cancer remained unexplored. We aimed to investigate the biological roles and underlying molecular mechanisms of NETO2 in pancreatic cancer. Materials and methods: Thirty paired pancreatic tumor tissue samples and corresponding nontumor tissues were obtained from 30 pancreatic cancer patients who did not receive preoperative chemotherapy or radiotherapy. The changes in multiple cellular functions associated with tumor progression were assessed after NETO2 knockdown/overexpression in pancreatic cancer cell lines. Additionally, a mouse-xenograft model was developed to verify the in vitro results. Results: NETO2 was upregulated in pancreatic tumor tissues. Elevated expression of NETO2 was not only associated with an advanced tumor stage, but was also a prediction of poor prognosis for pancreatic cancer patients. Knockdown of NETO2 in pancreatic cancer cell lines arrested the cell cycle and inhibited cell proliferation, colony formation, invasion, and migration; in contrast, overexpression of NETO2 had an opposite effect on all of these parameters. A STAT3 specific inhibitor, cryptotanshinone, reversed the tumor-promoting effects induced by NETO2 overexpression in pancreatic cancer. Western blot analysis showed that invasion and migration were closely related to epithelial–mesenchymal transition, and that the STAT3 signaling pathway was involved in NETO2 -mediated oncogenic transformation in pancreatic cancer cells. Furthermore, NETO2 knockdown significantly inhibited the growth of pancreatic tumor xenografts in nude mice. Conclusion: NETO2 has an important role in the progression and metastasis of pancreatic cancer and could serve as a novel candidate for targeted therapy of pancreatic cancer.

show abstract

ZFX Promotes Proliferation and Metastasis of Pancreatic Cancer Cells via the MAPK Pathway

Cited by 19 publications

References 24 publications

Liensinine inhibited gastric cancer cell growth through ROS generation and the PI3K/AKT pathway

Liensinine inhibited gastric cancer cell growth through ROS generation and the PI3K/AKT pathway

CCAT1 promotes triple-negative breast cancer progression by suppressing miR-218/ZFX signaling

<p><em>NETO2</em> promotes pancreatic cancer cell proliferation, invasion and migration via activation of the <em>STAT3</em> signaling pathway</p>

Contact Info

Product

Resources

About