Semaphorin 3 C enhances putative cancer stemness and accelerates peritoneal dissemination in pancreatic cancer

Purpose Semaphorins, axon guidance cues in neuronal network formation, have been implicated in cancer progression. We previously identified semaphorin 3 C (SEMA3C) as a secreted protein overexpressed in pancreatic ductal adenocarcinoma (PDAC). We, therefore, hypothesized that SEMA3C supports PDAC pr...

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Published inCancer cell international Vol. 23; no. 1; pp. 155 - 14
Main Authors Tomizawa, Satoshi, Takano, Shigetsugu, Eto, Ryotaro, Takayashiki, Tsukasa, Kuboki, Satoshi, Ohtsuka, Masayuki
Format Journal Article
LanguageEnglish
Published London BioMed Central 03.08.2023
BMC
Subjects
Adenocarcinoma
AKT protein
Antibodies
Axon guidance
Biomedical and Life Sciences
Biomedicine
Cancer Research
Cancer stemness
Cancer therapies
Cell Biology
Cell self-renewal
Chemoresistance
Colonies
Cytotoxicity
Dehydrogenases
Flow cytometry
Gemcitabine
Immunohistochemistry
Neural networks
Paclitaxel
Pancreatic cancer
Patients
Peritoneal dissemination
Peritoneum
Phosphorylation
Proteins
SEMA3C
Semaphorins
Software
TOR protein
Transplantation
United States > US
Japan
Cancer stemness
Peritoneal dissemination
SEMA3C
Pancreatic cancer
Chemoresistance
Online AccessGet full text
ISSN1475-2867
1475-2867
DOI10.1186/s12935-023-03008-3

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Abstract Purpose Semaphorins, axon guidance cues in neuronal network formation, have been implicated in cancer progression. We previously identified semaphorin 3 C (SEMA3C) as a secreted protein overexpressed in pancreatic ductal adenocarcinoma (PDAC). We, therefore, hypothesized that SEMA3C supports PDAC progression. In this study, we aimed to investigate the clinical features of SEMA3C, especially its association with chemo-resistance and peritoneal dissemination. Methods In resected PDAC tissues, we assessed the relationship between SEMA3C expression and clinicopathological features by immunohistochemistry. In vitro studies, we have shown invasion assay, pancreatosphere formation assay, colony formation assay, cytotoxicity assay, and activation of SEMA3C downstream targets (c-Met, Akt, mTOR). In vivo, we performed a preclinical trial to confirm the efficacy of SEMA3C shRNA knockdown and Gemcitabine and nab-Paclitaxel (GnP) in an orthotopic transplantation mouse model and in peritoneal dissemination mouse model. Results In resected PDAC tissues, SEMA3C expression correlated with invasion and peritoneal dissemination after surgery. SEMA3C promoted cell invasion, self-renewal, and colony formation in vitro. We further demonstrated that SEMA3C knockdown increased Gem-induced cytotoxicity by suppressing the activation of the Akt/mTOR pathway via the c-Met receptor. Combination therapy with SEMA3C knockdown and GnP reduced tumor growth and peritoneal dissemination. Conclusions SEMA3C enhances peritoneal dissemination by regulating putative cancer stemness and Gem resistance and activates phosphorylation of the Akt/mTOR pathway via c-Met. Our findings provide a new avenue for therapeutic strategies in regulating peritoneal dissemination during PDAC progression.
AbstractList PurposeSemaphorins, axon guidance cues in neuronal network formation, have been implicated in cancer progression. We previously identified semaphorin 3 C (SEMA3C) as a secreted protein overexpressed in pancreatic ductal adenocarcinoma (PDAC). We, therefore, hypothesized that SEMA3C supports PDAC progression. In this study, we aimed to investigate the clinical features of SEMA3C, especially its association with chemo-resistance and peritoneal dissemination.MethodsIn resected PDAC tissues, we assessed the relationship between SEMA3C expression and clinicopathological features by immunohistochemistry. In vitro studies, we have shown invasion assay, pancreatosphere formation assay, colony formation assay, cytotoxicity assay, and activation of SEMA3C downstream targets (c-Met, Akt, mTOR). In vivo, we performed a preclinical trial to confirm the efficacy of SEMA3C shRNA knockdown and Gemcitabine and nab-Paclitaxel (GnP) in an orthotopic transplantation mouse model and in peritoneal dissemination mouse model.ResultsIn resected PDAC tissues, SEMA3C expression correlated with invasion and peritoneal dissemination after surgery. SEMA3C promoted cell invasion, self-renewal, and colony formation in vitro. We further demonstrated that SEMA3C knockdown increased Gem-induced cytotoxicity by suppressing the activation of the Akt/mTOR pathway via the c-Met receptor. Combination therapy with SEMA3C knockdown and GnP reduced tumor growth and peritoneal dissemination.ConclusionsSEMA3C enhances peritoneal dissemination by regulating putative cancer stemness and Gem resistance and activates phosphorylation of the Akt/mTOR pathway via c-Met. Our findings provide a new avenue for therapeutic strategies in regulating peritoneal dissemination during PDAC progression.
Semaphorins, axon guidance cues in neuronal network formation, have been implicated in cancer progression. We previously identified semaphorin 3 C (SEMA3C) as a secreted protein overexpressed in pancreatic ductal adenocarcinoma (PDAC). We, therefore, hypothesized that SEMA3C supports PDAC progression. In this study, we aimed to investigate the clinical features of SEMA3C, especially its association with chemo-resistance and peritoneal dissemination. In resected PDAC tissues, we assessed the relationship between SEMA3C expression and clinicopathological features by immunohistochemistry. In vitro studies, we have shown invasion assay, pancreatosphere formation assay, colony formation assay, cytotoxicity assay, and activation of SEMA3C downstream targets (c-Met, Akt, mTOR). In vivo, we performed a preclinical trial to confirm the efficacy of SEMA3C shRNA knockdown and Gemcitabine and nab-Paclitaxel (GnP) in an orthotopic transplantation mouse model and in peritoneal dissemination mouse model. In resected PDAC tissues, SEMA3C expression correlated with invasion and peritoneal dissemination after surgery. SEMA3C promoted cell invasion, self-renewal, and colony formation in vitro. We further demonstrated that SEMA3C knockdown increased Gem-induced cytotoxicity by suppressing the activation of the Akt/mTOR pathway via the c-Met receptor. Combination therapy with SEMA3C knockdown and GnP reduced tumor growth and peritoneal dissemination. SEMA3C enhances peritoneal dissemination by regulating putative cancer stemness and Gem resistance and activates phosphorylation of the Akt/mTOR pathway via c-Met. Our findings provide a new avenue for therapeutic strategies in regulating peritoneal dissemination during PDAC progression.
Purpose Semaphorins, axon guidance cues in neuronal network formation, have been implicated in cancer progression. We previously identified semaphorin 3 C (SEMA3C) as a secreted protein overexpressed in pancreatic ductal adenocarcinoma (PDAC). We, therefore, hypothesized that SEMA3C supports PDAC progression. In this study, we aimed to investigate the clinical features of SEMA3C, especially its association with chemo-resistance and peritoneal dissemination. Methods In resected PDAC tissues, we assessed the relationship between SEMA3C expression and clinicopathological features by immunohistochemistry. In vitro studies, we have shown invasion assay, pancreatosphere formation assay, colony formation assay, cytotoxicity assay, and activation of SEMA3C downstream targets (c-Met, Akt, mTOR). In vivo, we performed a preclinical trial to confirm the efficacy of SEMA3C shRNA knockdown and Gemcitabine and nab-Paclitaxel (GnP) in an orthotopic transplantation mouse model and in peritoneal dissemination mouse model. Results In resected PDAC tissues, SEMA3C expression correlated with invasion and peritoneal dissemination after surgery. SEMA3C promoted cell invasion, self-renewal, and colony formation in vitro. We further demonstrated that SEMA3C knockdown increased Gem-induced cytotoxicity by suppressing the activation of the Akt/mTOR pathway via the c-Met receptor. Combination therapy with SEMA3C knockdown and GnP reduced tumor growth and peritoneal dissemination. Conclusions SEMA3C enhances peritoneal dissemination by regulating putative cancer stemness and Gem resistance and activates phosphorylation of the Akt/mTOR pathway via c-Met. Our findings provide a new avenue for therapeutic strategies in regulating peritoneal dissemination during PDAC progression.
Semaphorins, axon guidance cues in neuronal network formation, have been implicated in cancer progression. We previously identified semaphorin 3 C (SEMA3C) as a secreted protein overexpressed in pancreatic ductal adenocarcinoma (PDAC). We, therefore, hypothesized that SEMA3C supports PDAC progression. In this study, we aimed to investigate the clinical features of SEMA3C, especially its association with chemo-resistance and peritoneal dissemination.PURPOSESemaphorins, axon guidance cues in neuronal network formation, have been implicated in cancer progression. We previously identified semaphorin 3 C (SEMA3C) as a secreted protein overexpressed in pancreatic ductal adenocarcinoma (PDAC). We, therefore, hypothesized that SEMA3C supports PDAC progression. In this study, we aimed to investigate the clinical features of SEMA3C, especially its association with chemo-resistance and peritoneal dissemination.In resected PDAC tissues, we assessed the relationship between SEMA3C expression and clinicopathological features by immunohistochemistry. In vitro studies, we have shown invasion assay, pancreatosphere formation assay, colony formation assay, cytotoxicity assay, and activation of SEMA3C downstream targets (c-Met, Akt, mTOR). In vivo, we performed a preclinical trial to confirm the efficacy of SEMA3C shRNA knockdown and Gemcitabine and nab-Paclitaxel (GnP) in an orthotopic transplantation mouse model and in peritoneal dissemination mouse model.METHODSIn resected PDAC tissues, we assessed the relationship between SEMA3C expression and clinicopathological features by immunohistochemistry. In vitro studies, we have shown invasion assay, pancreatosphere formation assay, colony formation assay, cytotoxicity assay, and activation of SEMA3C downstream targets (c-Met, Akt, mTOR). In vivo, we performed a preclinical trial to confirm the efficacy of SEMA3C shRNA knockdown and Gemcitabine and nab-Paclitaxel (GnP) in an orthotopic transplantation mouse model and in peritoneal dissemination mouse model.In resected PDAC tissues, SEMA3C expression correlated with invasion and peritoneal dissemination after surgery. SEMA3C promoted cell invasion, self-renewal, and colony formation in vitro. We further demonstrated that SEMA3C knockdown increased Gem-induced cytotoxicity by suppressing the activation of the Akt/mTOR pathway via the c-Met receptor. Combination therapy with SEMA3C knockdown and GnP reduced tumor growth and peritoneal dissemination.RESULTSIn resected PDAC tissues, SEMA3C expression correlated with invasion and peritoneal dissemination after surgery. SEMA3C promoted cell invasion, self-renewal, and colony formation in vitro. We further demonstrated that SEMA3C knockdown increased Gem-induced cytotoxicity by suppressing the activation of the Akt/mTOR pathway via the c-Met receptor. Combination therapy with SEMA3C knockdown and GnP reduced tumor growth and peritoneal dissemination.SEMA3C enhances peritoneal dissemination by regulating putative cancer stemness and Gem resistance and activates phosphorylation of the Akt/mTOR pathway via c-Met. Our findings provide a new avenue for therapeutic strategies in regulating peritoneal dissemination during PDAC progression.CONCLUSIONSSEMA3C enhances peritoneal dissemination by regulating putative cancer stemness and Gem resistance and activates phosphorylation of the Akt/mTOR pathway via c-Met. Our findings provide a new avenue for therapeutic strategies in regulating peritoneal dissemination during PDAC progression.
Abstract Purpose Semaphorins, axon guidance cues in neuronal network formation, have been implicated in cancer progression. We previously identified semaphorin 3 C (SEMA3C) as a secreted protein overexpressed in pancreatic ductal adenocarcinoma (PDAC). We, therefore, hypothesized that SEMA3C supports PDAC progression. In this study, we aimed to investigate the clinical features of SEMA3C, especially its association with chemo-resistance and peritoneal dissemination. Methods In resected PDAC tissues, we assessed the relationship between SEMA3C expression and clinicopathological features by immunohistochemistry. In vitro studies, we have shown invasion assay, pancreatosphere formation assay, colony formation assay, cytotoxicity assay, and activation of SEMA3C downstream targets (c-Met, Akt, mTOR). In vivo, we performed a preclinical trial to confirm the efficacy of SEMA3C shRNA knockdown and Gemcitabine and nab-Paclitaxel (GnP) in an orthotopic transplantation mouse model and in peritoneal dissemination mouse model. Results In resected PDAC tissues, SEMA3C expression correlated with invasion and peritoneal dissemination after surgery. SEMA3C promoted cell invasion, self-renewal, and colony formation in vitro. We further demonstrated that SEMA3C knockdown increased Gem-induced cytotoxicity by suppressing the activation of the Akt/mTOR pathway via the c-Met receptor. Combination therapy with SEMA3C knockdown and GnP reduced tumor growth and peritoneal dissemination. Conclusions SEMA3C enhances peritoneal dissemination by regulating putative cancer stemness and Gem resistance and activates phosphorylation of the Akt/mTOR pathway via c-Met. Our findings provide a new avenue for therapeutic strategies in regulating peritoneal dissemination during PDAC progression.
ArticleNumber 155
Author Tomizawa, Satoshi
Eto, Ryotaro
Ohtsuka, Masayuki
Takano, Shigetsugu
Takayashiki, Tsukasa
Kuboki, Satoshi
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Cites_doi 10.1002/bjs.11295
10.1016/j.jss.2012.05.065
10.1053/j.gastro.2011.08.009
10.1016/j.freeradbiomed.2011.03.007
10.15252/emmm.201707689
10.1016/j.ajhg.2015.02.014
10.1369/0022155417742897
10.3748/wjg.v22.i30.6829
10.1073/pnas.0912589107
10.3389/fonc.2022.890154
10.1158/1078-0432.CCR-18-0290
10.1158/0008-5472.CAN-06-2030
10.1126/scisignal.aaa5823
10.1097/SLA.0000000000002234
10.1016/j.stem.2007.06.002
10.1053/j.gastro.2019.05.065
10.1053/j.gastro.2013.01.072
10.1016/j.jtho.2020.01.027
10.3390/biomedicines6020042
10.1038/s41573-020-0075-7
10.1016/j.omtn.2020.10.001
10.1101/gad.263327.115
10.3322/caac.21708
10.1007/s13402-021-00614-z
10.3390/antibiotics11111662
10.1038/nature11547
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Issue 1
Keywords Cancer stemness
Peritoneal dissemination
SEMA3C
Pancreatic cancer
Chemoresistance
Language English
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References 3008_CR16
G Hu (3008_CR20) 2012; 40
C Li (3008_CR14) 2011; 141
CTR Langer (3008_CR24) 2020; 19
M Kanda (3008_CR27) 2020; 22
EV Abel (3008_CR15) 2013; 144
P Jamme (3008_CR23) 2020; 15
K Foley (3008_CR18) 2015; 8
C Li (3008_CR12) 2007; 67
M Tanaka (3008_CR3) 2019; 106
RL Siegel (3008_CR1) 2022; 72
MG Espey (3008_CR21) 2011; 50
J Hao (3008_CR7) 2018; 6
P Nasarre (3008_CR6) 2014; 7
S Kagawa (3008_CR22) 2012; 178
NR Jurcak (3008_CR19) 2019; 157
PC Hermann (3008_CR13) 2007; 1
JOAM van Baal (3008_CR5) 2018; 66
I Peran (3008_CR11) 2018; 24
M Traykovska (3008_CR25) 2022; 11
M Kanda (3008_CR4) 2016; 22
M Rovira (3008_CR9) 2010; 107
S Takano (3008_CR10) 2016; 30
Q Jiang (3008_CR17) 2015; 96
VP Groot (3008_CR2) 2018; 267
JW Peacock (3008_CR26) 2018; 10
R Shimazaki (3008_CR8) 2021; 44
D Zhang (3008_CR28) 2022; 16
References_xml – volume: 106
  start-page: 1590
  year: 2019
  ident: 3008_CR3
  publication-title: Br J Surg
  doi: 10.1002/bjs.11295
– volume: 178
  start-page: 758
  year: 2012
  ident: 3008_CR22
  publication-title: J Surg Res
  doi: 10.1016/j.jss.2012.05.065
– volume: 141
  start-page: 2218
  year: 2011
  ident: 3008_CR14
  publication-title: Gastroenterology
  doi: 10.1053/j.gastro.2011.08.009
– volume: 50
  start-page: 1610
  year: 2011
  ident: 3008_CR21
  publication-title: Free Radic Biol Med
  doi: 10.1016/j.freeradbiomed.2011.03.007
– volume: 10
  start-page: 219
  year: 2018
  ident: 3008_CR26
  publication-title: EMBO Mol Med
  doi: 10.15252/emmm.201707689
– volume: 96
  start-page: 581
  year: 2015
  ident: 3008_CR17
  publication-title: Am J Hum Genet
  doi: 10.1016/j.ajhg.2015.02.014
– volume: 7
  start-page: 1663
  year: 2014
  ident: 3008_CR6
  publication-title: Onco Targets Ther
– volume: 66
  start-page: 67
  year: 2018
  ident: 3008_CR5
  publication-title: J Histochem Cytochem
  doi: 10.1369/0022155417742897
– volume: 22
  start-page: 6829
  year: 2016
  ident: 3008_CR4
  publication-title: World J Gastroenterol
  doi: 10.3748/wjg.v22.i30.6829
– volume: 107
  start-page: 75
  year: 2010
  ident: 3008_CR9
  publication-title: Proc Natl Acad Sci U S A
  doi: 10.1073/pnas.0912589107
– volume: 16
  start-page: 890154
  year: 2022
  ident: 3008_CR28
  publication-title: Front Oncol
  doi: 10.3389/fonc.2022.890154
– volume: 24
  start-page: 3813
  year: 2018
  ident: 3008_CR11
  publication-title: Clin Cancer Res
  doi: 10.1158/1078-0432.CCR-18-0290
– volume: 67
  start-page: 1030
  year: 2007
  ident: 3008_CR12
  publication-title: Cancer Res
  doi: 10.1158/0008-5472.CAN-06-2030
– volume: 8
  start-page: ra77
  year: 2015
  ident: 3008_CR18
  publication-title: Sci Signal
  doi: 10.1126/scisignal.aaa5823
– volume: 267
  start-page: 936
  year: 2018
  ident: 3008_CR2
  publication-title: Ann Surg
  doi: 10.1097/SLA.0000000000002234
– volume: 1
  start-page: 313
  year: 2007
  ident: 3008_CR13
  publication-title: Cell Stem Cell
  doi: 10.1016/j.stem.2007.06.002
– volume: 157
  start-page: 838
  year: 2019
  ident: 3008_CR19
  publication-title: Gastroenterology
  doi: 10.1053/j.gastro.2019.05.065
– volume: 144
  start-page: 1241
  year: 2013
  ident: 3008_CR15
  publication-title: Gastroenterology
  doi: 10.1053/j.gastro.2013.01.072
– volume: 15
  start-page: 741
  year: 2020
  ident: 3008_CR23
  publication-title: J Thorac Oncol
  doi: 10.1016/j.jtho.2020.01.027
– volume: 6
  start-page: 42
  year: 2018
  ident: 3008_CR7
  publication-title: Biomedicines
  doi: 10.3390/biomedicines6020042
– volume: 19
  start-page: 673
  year: 2020
  ident: 3008_CR24
  publication-title: Nat Rev Drug Discov
  doi: 10.1038/s41573-020-0075-7
– volume: 22
  start-page: 791
  year: 2020
  ident: 3008_CR27
  publication-title: Mol Ther Nucleic Acids
  doi: 10.1016/j.omtn.2020.10.001
– volume: 30
  start-page: 233
  year: 2016
  ident: 3008_CR10
  publication-title: Genes Dev
  doi: 10.1101/gad.263327.115
– volume: 72
  start-page: 7
  year: 2022
  ident: 3008_CR1
  publication-title: CA Cancer J Clin
  doi: 10.3322/caac.21708
– volume: 44
  start-page: 937
  year: 2021
  ident: 3008_CR8
  publication-title: Cell Oncol (Dordr)
  doi: 10.1007/s13402-021-00614-z
– volume: 40
  start-page: 798
  year: 2012
  ident: 3008_CR20
  publication-title: Int J Oncol
– volume: 11
  start-page: 1662
  year: 2022
  ident: 3008_CR25
  publication-title: Antibiot (Basel)
  doi: 10.3390/antibiotics11111662
– ident: 3008_CR16
  doi: 10.1038/nature11547
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Snippet Purpose Semaphorins, axon guidance cues in neuronal network formation, have been implicated in cancer progression. We previously identified semaphorin 3 C...
Semaphorins, axon guidance cues in neuronal network formation, have been implicated in cancer progression. We previously identified semaphorin 3 C (SEMA3C) as...
PurposeSemaphorins, axon guidance cues in neuronal network formation, have been implicated in cancer progression. We previously identified semaphorin 3 C...
Semaphorins, axon guidance cues in neuronal network formation, have been implicated in cancer progression. We previously identified semaphorin 3 C (SEMA3C) as...
Abstract Purpose Semaphorins, axon guidance cues in neuronal network formation, have been implicated in cancer progression. We previously identified semaphorin...
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SubjectTerms Adenocarcinoma
AKT protein
Antibodies
Axon guidance
Biomedical and Life Sciences
Biomedicine
Cancer Research
Cancer stemness
Cancer therapies
Cell Biology
Cell self-renewal
Chemoresistance
Colonies
Cytotoxicity
Dehydrogenases
Flow cytometry
Gemcitabine
Immunohistochemistry
Neural networks
Paclitaxel
Pancreatic cancer
Patients
Peritoneal dissemination
Peritoneum
Phosphorylation
Proteins
SEMA3C
Semaphorins
Software
TOR protein
Transplantation
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Title Semaphorin 3 C enhances putative cancer stemness and accelerates peritoneal dissemination in pancreatic cancer
URI https://link.springer.com/article/10.1186/s12935-023-03008-3
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