<i>Neurotensin</i>, a novel target of Wnt/β‐catenin pathway, promotes growth of neuroendocrine tumor cells

Kim, Ji Tae; Liu, Chunming; Zaytseva, Yekaterina Y.; Weiss, Heidi L.; Townsend, Courtney M.; Evers, B. Mark

doi:10.1002/ijc.29123

Cited by 33 publications

(46 citation statements)

References 24 publications

(58 reference statements)

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“…Neurotensin is regulated by the Wnt/b-catenin signaling pathway in human neuroendocrine tumors. 34 This pathway is a fundamental mechanism for cell proliferation, cell polarity, and cell-fate determination during embryonic development and tissue homeostasis. 35 In prostate cancer, the Wnt/b-catenin Figure 6 Invasion assay was performed by using a Boyden chamber as described in Figure 3b.…”

Section: Gelsolin-mediated Invasion Of Prostate Cancer K Hashimoto Et Almentioning

confidence: 99%

The potential of neurotensin secreted from neuroendocrine tumor cells to promote gelsolin-mediated invasiveness of prostate adenocarcinoma cells

Hashimoto

Kyoda

Tanaka

et al. 2015

Laboratory Investigation

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Neuroendocrine (NE) cells in prostate cancer have been shown to be associated with the progression of prostate cancer. However, little is known about the molecular basis of this association. We have previously demonstrated that NE cells promote metastasis of a human prostate cancer cell line (LNCaP) with overexpression of the gelsolin gene. The purpose of this study was to investigate the interactions between NE cells and LNCaP cells and the involvement of gelsolin in contributing to the invasive potential of LNCaP cells. In addition, we examined whether neurotensin induced gelsolin-mediated invasion. We used the NE cell line NE-CS that was established from the prostate of the LPB-Tag 12T-10 transgenic mouse. Small interfering RNA (siRNA) targeting gelsolin or not targeting it was transfected into LNCaP cells.

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Section: Gelsolin-mediated Invasion Of Prostate Cancer K Hashimoto Et Almentioning

confidence: 99%

The potential of neurotensin secreted from neuroendocrine tumor cells to promote gelsolin-mediated invasiveness of prostate adenocarcinoma cells

Hashimoto

Kyoda

Tanaka

et al. 2015

Laboratory Investigation

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“…There is also evidence suggesting that menin (encoded by MEN1) activates the Wnt signaling pathway resulting in inhibition of islet tumor cell proliferation in a mouse model 244 . Further, it was recently been demonstrated that neurotensin is a target of the Wnt signaling pathway and promotes growth of pancreatic neuroendocrine cells 245 . These observations strengthen the idea of the Wnt signaling pathway as a potential target for molecular markers of prognosis in patients with sporadic nonfunctioning PNEN.…”

Section: Genomic Expression Profiling In Pnensmentioning

confidence: 99%

Long‐Term Outcome of Laparoscopic Surgery for Pancreatic Neuroendocrine Tumors

et al. 2012

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“…Recently, it has been demostrated that NTSR1 is a direct target of the Wnt/APC oncogenic pathways connected with the β-catenin/Tcf transcriptional complex [14]. And excitingly, NTS is also a direct target of the Wnt/β-catenin pathway and may be a mediator for neuroendocrine tumor cell growth [4]. …”

Section: Introductionmentioning

confidence: 99%

A Novel Positive Feedback Loop Between NTSR1 and Wnt/β-Catenin Contributes to Tumor Growth of Glioblastoma

Xiao¹,

Zeng²,

Wang³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Neurotensin (NTS), an intestinal hormone, is profoundly implicated in cancer progression through binding its primary receptor NTSR1. The conserved Wnt/β-Catenin pathway regulates cell proliferation and differentiation via activation of the β-catenin/T-cell factor (TCF) complex and subsequent modulation of a set of target genes. In this study, we aimed to uncover the potential connection between NTS/NTSR1 signaling and Wnt/β-Catenin pathway. Methods: Genetic silencing, pharmacological inhibition and gain-of-function studies as well as bioinformatic analysis were performed to uncover the link between NTS/ NTSR1 signaling and Wnt/β-Catenin pathway. Two inhibitors were used in vivo to evaluate the efficiency of targeting NTS/NTSR1 signaling or Wnt/β-Catenin pathway. Results: We found that NTS/NTSR1 induced the activation of mitogen-activated protein kinase (MAPK) and the NF-κB pathway, which further promoted the expression of Wnt proteins, including Wnt1, Wnt3a and Wnt5a. Meanwhile, the mRNA and protein expression levels of NTSR1 were increased by the Wnt pathway activator Wnt3a and decreased by the Wnt inhibitor iCRT3 in glioblastoma cells. Furthermore, pharmacological inhibition of NTS/NTSR1 or Wnt/β-Catenin signaling suppressed tumor growth in vitro and in vivo. Conclusion: These results reveal a positive feedback loop between NTS/NTSR1 and Wnt/β-Catenin signaling in glioblastoma cells that might be important for tumor development and provide potential therapeutic targets for glioblastoma.

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Neurotensin, a novel target of Wnt/β‐catenin pathway, promotes growth of neuroendocrine tumor cells

Cited by 33 publications

References 24 publications

The potential of neurotensin secreted from neuroendocrine tumor cells to promote gelsolin-mediated invasiveness of prostate adenocarcinoma cells

The potential of neurotensin secreted from neuroendocrine tumor cells to promote gelsolin-mediated invasiveness of prostate adenocarcinoma cells

Long‐Term Outcome of Laparoscopic Surgery for Pancreatic Neuroendocrine Tumors

A Novel Positive Feedback Loop Between NTSR1 and Wnt/β-Catenin Contributes to Tumor Growth of Glioblastoma

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