Glucose transporter 1 regulates the proliferation and cisplatin sensitivity of esophageal cancer
Glucose transporter 1 (GLUT1) expression is a prognostic marker for esophageal squamous cell carcinoma (ESCC). Recent work on GLUT1 and development of specific inhibitors supports the feasibility of GLUT1 inhibition as a treatment for various cancers. The anti–proliferative effects of GLUT1‐specific...
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| Published in | Cancer science Vol. 110; no. 5; pp. 1705 - 1714 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
John Wiley & Sons, Inc
01.05.2019
John Wiley and Sons Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1347-9032 1349-7006 1349-7006 |
| DOI | 10.1111/cas.13995 |
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| Abstract | Glucose transporter 1 (GLUT1) expression is a prognostic marker for esophageal squamous cell carcinoma (ESCC). Recent work on GLUT1 and development of specific inhibitors supports the feasibility of GLUT1 inhibition as a treatment for various cancers. The anti–proliferative effects of GLUT1‐specific small interfering RNA (siRNA) and a GLUT1 inhibitor were evaluated in ESCC cell lines. Expression of pro–proliferative and anti–proliferative signaling and effector molecules was examined by western blotting and quantitative RT‐PCR. GLUT1 expression in pretreatment clinical biopsy samples was measured by immunohistochemistry and correlated with various clinicopathological parameters and response to chemotherapy. The reduction in standardized uptake value (SUV) of 18F‐fluoro‐deoxyglucose was calculated using the formula: ([pretreatment SUVmax – posttreatment SUVmax]/pretreatment SUVmax) × 100. GLUT1‐specific siRNA expression in ESCC cells inhibited their proliferation, increased expression of p27kip, and decreased expression of cyclin‐dependent kinase 6, pyruvate kinase muscle isozyme M2, lactate dehydrogenase A and phospho‐ERK1/2. Suppression of GLUT1 by siRNA increased low‐dose cisplatin‐induced inhibition of proliferation of TE‐11 ESCC cells, which express high GLUT1 levels. Similarly, BAY‐876, a GLUT1 inhibitor, enhanced cisplatin‐mediated inhibition of ESCC cell proliferation. GLUT1 expression in pretreatment biopsy samples was associated with the response to chemotherapy as well as the pathological tumor stage and histological response grade after esophagectomy. Finally, GLUT1‐negative tumors showed a significantly larger reduction in SUVmax (61.2% ± 4.5%) compared with GLUT1‐positive tumors (46.2% ± 4.4%). GLUT1 expression may be a surrogate marker of response to chemotherapy, and inhibition of GLUT1 may be a potential novel therapy for ESCC patients.
Recent work on GLUT1 and development of specific inhibitors supports the feasibility of GLUT1 inhibition as a treatment for various cancers. This study demonstrated that downregulation of GLUT1 expression had a strong anti–proliferative effect in ESCC cells and also improved their sensitivity to cisplatin. GLUT1 expression may be a surrogate marker of response to chemotherapy, and inhibition of GLUT1 may be a potential novel therapy for ESCC patients. |
|---|---|
| AbstractList | Glucose transporter 1 (
GLUT
1) expression is a prognostic marker for esophageal squamous cell carcinoma (
ESCC
). Recent work on
GLUT
1 and development of specific inhibitors supports the feasibility of
GLUT
1 inhibition as a treatment for various cancers. The anti–proliferative effects of
GLUT
1‐specific small interfering
RNA
(si
RNA
) and a
GLUT
1 inhibitor were evaluated in
ESCC
cell lines. Expression of pro–proliferative and anti–proliferative signaling and effector molecules was examined by western blotting and quantitative
RT
‐
PCR
.
GLUT
1 expression in pretreatment clinical biopsy samples was measured by immunohistochemistry and correlated with various clinicopathological parameters and response to chemotherapy. The reduction in standardized uptake value (
SUV
) of
18
F‐fluoro‐deoxyglucose was calculated using the formula: ([pretreatment
SUV
max
– posttreatment
SUV
max
]/pretreatment
SUV
max
) × 100.
GLUT
1‐specific si
RNA
expression in
ESCC
cells inhibited their proliferation, increased expression of p27kip, and decreased expression of cyclin‐dependent kinase 6, pyruvate kinase muscle isozyme M2, lactate dehydrogenase A and phospho‐
ERK
1/2. Suppression of
GLUT
1 by si
RNA
increased low‐dose cisplatin‐induced inhibition of proliferation of
TE
‐11
ESCC
cells, which express high
GLUT
1 levels. Similarly,
BAY
‐876, a
GLUT
1 inhibitor, enhanced cisplatin‐mediated inhibition of
ESCC
cell proliferation.
GLUT
1 expression in pretreatment biopsy samples was associated with the response to chemotherapy as well as the pathological tumor stage and histological response grade after esophagectomy. Finally,
GLUT
1‐negative tumors showed a significantly larger reduction in
SUV
max
(61.2% ± 4.5%) compared with
GLUT
1‐positive tumors (46.2% ± 4.4%).
GLUT
1 expression may be a surrogate marker of response to chemotherapy, and inhibition of
GLUT
1 may be a potential novel therapy for
ESCC
patients. Glucose transporter 1 (GLUT1) expression is a prognostic marker for esophageal squamous cell carcinoma (ESCC). Recent work on GLUT1 and development of specific inhibitors supports the feasibility of GLUT1 inhibition as a treatment for various cancers. The anti-proliferative effects of GLUT1-specific small interfering RNA (siRNA) and a GLUT1 inhibitor were evaluated in ESCC cell lines. Expression of pro-proliferative and anti-proliferative signaling and effector molecules was examined by western blotting and quantitative RT-PCR. GLUT1 expression in pretreatment clinical biopsy samples was measured by immunohistochemistry and correlated with various clinicopathological parameters and response to chemotherapy. The reduction in standardized uptake value (SUV) of F-fluoro-deoxyglucose was calculated using the formula: ([pretreatment SUV - posttreatment SUV ]/pretreatment SUV ) × 100. GLUT1-specific siRNA expression in ESCC cells inhibited their proliferation, increased expression of p27kip, and decreased expression of cyclin-dependent kinase 6, pyruvate kinase muscle isozyme M2, lactate dehydrogenase A and phospho-ERK1/2. Suppression of GLUT1 by siRNA increased low-dose cisplatin-induced inhibition of proliferation of TE-11 ESCC cells, which express high GLUT1 levels. Similarly, BAY-876, a GLUT1 inhibitor, enhanced cisplatin-mediated inhibition of ESCC cell proliferation. GLUT1 expression in pretreatment biopsy samples was associated with the response to chemotherapy as well as the pathological tumor stage and histological response grade after esophagectomy. Finally, GLUT1-negative tumors showed a significantly larger reduction in SUV (61.2% ± 4.5%) compared with GLUT1-positive tumors (46.2% ± 4.4%). GLUT1 expression may be a surrogate marker of response to chemotherapy, and inhibition of GLUT1 may be a potential novel therapy for ESCC patients. Glucose transporter 1 (GLUT1) expression is a prognostic marker for esophageal squamous cell carcinoma (ESCC). Recent work on GLUT1 and development of specific inhibitors supports the feasibility of GLUT1 inhibition as a treatment for various cancers. The anti-proliferative effects of GLUT1-specific small interfering RNA (siRNA) and a GLUT1 inhibitor were evaluated in ESCC cell lines. Expression of pro-proliferative and anti-proliferative signaling and effector molecules was examined by western blotting and quantitative RT-PCR. GLUT1 expression in pretreatment clinical biopsy samples was measured by immunohistochemistry and correlated with various clinicopathological parameters and response to chemotherapy. The reduction in standardized uptake value (SUV) of 18 F-fluoro-deoxyglucose was calculated using the formula: ([pretreatment SUVmax - posttreatment SUVmax ]/pretreatment SUVmax ) × 100. GLUT1-specific siRNA expression in ESCC cells inhibited their proliferation, increased expression of p27kip, and decreased expression of cyclin-dependent kinase 6, pyruvate kinase muscle isozyme M2, lactate dehydrogenase A and phospho-ERK1/2. Suppression of GLUT1 by siRNA increased low-dose cisplatin-induced inhibition of proliferation of TE-11 ESCC cells, which express high GLUT1 levels. Similarly, BAY-876, a GLUT1 inhibitor, enhanced cisplatin-mediated inhibition of ESCC cell proliferation. GLUT1 expression in pretreatment biopsy samples was associated with the response to chemotherapy as well as the pathological tumor stage and histological response grade after esophagectomy. Finally, GLUT1-negative tumors showed a significantly larger reduction in SUVmax (61.2% ± 4.5%) compared with GLUT1-positive tumors (46.2% ± 4.4%). GLUT1 expression may be a surrogate marker of response to chemotherapy, and inhibition of GLUT1 may be a potential novel therapy for ESCC patients.Glucose transporter 1 (GLUT1) expression is a prognostic marker for esophageal squamous cell carcinoma (ESCC). Recent work on GLUT1 and development of specific inhibitors supports the feasibility of GLUT1 inhibition as a treatment for various cancers. The anti-proliferative effects of GLUT1-specific small interfering RNA (siRNA) and a GLUT1 inhibitor were evaluated in ESCC cell lines. Expression of pro-proliferative and anti-proliferative signaling and effector molecules was examined by western blotting and quantitative RT-PCR. GLUT1 expression in pretreatment clinical biopsy samples was measured by immunohistochemistry and correlated with various clinicopathological parameters and response to chemotherapy. The reduction in standardized uptake value (SUV) of 18 F-fluoro-deoxyglucose was calculated using the formula: ([pretreatment SUVmax - posttreatment SUVmax ]/pretreatment SUVmax ) × 100. GLUT1-specific siRNA expression in ESCC cells inhibited their proliferation, increased expression of p27kip, and decreased expression of cyclin-dependent kinase 6, pyruvate kinase muscle isozyme M2, lactate dehydrogenase A and phospho-ERK1/2. Suppression of GLUT1 by siRNA increased low-dose cisplatin-induced inhibition of proliferation of TE-11 ESCC cells, which express high GLUT1 levels. Similarly, BAY-876, a GLUT1 inhibitor, enhanced cisplatin-mediated inhibition of ESCC cell proliferation. GLUT1 expression in pretreatment biopsy samples was associated with the response to chemotherapy as well as the pathological tumor stage and histological response grade after esophagectomy. Finally, GLUT1-negative tumors showed a significantly larger reduction in SUVmax (61.2% ± 4.5%) compared with GLUT1-positive tumors (46.2% ± 4.4%). GLUT1 expression may be a surrogate marker of response to chemotherapy, and inhibition of GLUT1 may be a potential novel therapy for ESCC patients. Glucose transporter 1 (GLUT1) expression is a prognostic marker for esophageal squamous cell carcinoma (ESCC). Recent work on GLUT1 and development of specific inhibitors supports the feasibility of GLUT1 inhibition as a treatment for various cancers. The anti–proliferative effects of GLUT1‐specific small interfering RNA (siRNA) and a GLUT1 inhibitor were evaluated in ESCC cell lines. Expression of pro–proliferative and anti–proliferative signaling and effector molecules was examined by western blotting and quantitative RT‐PCR. GLUT1 expression in pretreatment clinical biopsy samples was measured by immunohistochemistry and correlated with various clinicopathological parameters and response to chemotherapy. The reduction in standardized uptake value (SUV) of 18F‐fluoro‐deoxyglucose was calculated using the formula: ([pretreatment SUVmax – posttreatment SUVmax]/pretreatment SUVmax) × 100. GLUT1‐specific siRNA expression in ESCC cells inhibited their proliferation, increased expression of p27kip, and decreased expression of cyclin‐dependent kinase 6, pyruvate kinase muscle isozyme M2, lactate dehydrogenase A and phospho‐ERK1/2. Suppression of GLUT1 by siRNA increased low‐dose cisplatin‐induced inhibition of proliferation of TE‐11 ESCC cells, which express high GLUT1 levels. Similarly, BAY‐876, a GLUT1 inhibitor, enhanced cisplatin‐mediated inhibition of ESCC cell proliferation. GLUT1 expression in pretreatment biopsy samples was associated with the response to chemotherapy as well as the pathological tumor stage and histological response grade after esophagectomy. Finally, GLUT1‐negative tumors showed a significantly larger reduction in SUVmax (61.2% ± 4.5%) compared with GLUT1‐positive tumors (46.2% ± 4.4%). GLUT1 expression may be a surrogate marker of response to chemotherapy, and inhibition of GLUT1 may be a potential novel therapy for ESCC patients. Recent work on GLUT1 and development of specific inhibitors supports the feasibility of GLUT1 inhibition as a treatment for various cancers. This study demonstrated that downregulation of GLUT1 expression had a strong anti–proliferative effect in ESCC cells and also improved their sensitivity to cisplatin. GLUT1 expression may be a surrogate marker of response to chemotherapy, and inhibition of GLUT1 may be a potential novel therapy for ESCC patients. Glucose transporter 1 (GLUT1) expression is a prognostic marker for esophageal squamous cell carcinoma (ESCC). Recent work on GLUT1 and development of specific inhibitors supports the feasibility of GLUT1 inhibition as a treatment for various cancers. The anti–proliferative effects of GLUT1‐specific small interfering RNA (siRNA) and a GLUT1 inhibitor were evaluated in ESCC cell lines. Expression of pro–proliferative and anti–proliferative signaling and effector molecules was examined by western blotting and quantitative RT‐PCR. GLUT1 expression in pretreatment clinical biopsy samples was measured by immunohistochemistry and correlated with various clinicopathological parameters and response to chemotherapy. The reduction in standardized uptake value (SUV) of 18F‐fluoro‐deoxyglucose was calculated using the formula: ([pretreatment SUVmax – posttreatment SUVmax]/pretreatment SUVmax) × 100. GLUT1‐specific siRNA expression in ESCC cells inhibited their proliferation, increased expression of p27kip, and decreased expression of cyclin‐dependent kinase 6, pyruvate kinase muscle isozyme M2, lactate dehydrogenase A and phospho‐ERK1/2. Suppression of GLUT1 by siRNA increased low‐dose cisplatin‐induced inhibition of proliferation of TE‐11 ESCC cells, which express high GLUT1 levels. Similarly, BAY‐876, a GLUT1 inhibitor, enhanced cisplatin‐mediated inhibition of ESCC cell proliferation. GLUT1 expression in pretreatment biopsy samples was associated with the response to chemotherapy as well as the pathological tumor stage and histological response grade after esophagectomy. Finally, GLUT1‐negative tumors showed a significantly larger reduction in SUVmax (61.2% ± 4.5%) compared with GLUT1‐positive tumors (46.2% ± 4.4%). GLUT1 expression may be a surrogate marker of response to chemotherapy, and inhibition of GLUT1 may be a potential novel therapy for ESCC patients. |
| Author | Ogata, Yoko Miyamoto, Yuji Yoshida, Naoya Ishimoto, Takatsugu Baba, Hideo Hiyoshi, Yukiharu Sawayama, Hiroshi Mima, Kosuke Iwatsuki, Masaaki Baba, Yoshifumi |
| AuthorAffiliation | 1 Department of Gastroenterological Surgery Graduate School of Medical Sciences Kumamoto University Kumamoto Japan |
| AuthorAffiliation_xml | – name: 1 Department of Gastroenterological Surgery Graduate School of Medical Sciences Kumamoto University Kumamoto Japan |
| Author_xml | – sequence: 1 givenname: Hiroshi surname: Sawayama fullname: Sawayama, Hiroshi organization: Kumamoto University – sequence: 2 givenname: Yoko surname: Ogata fullname: Ogata, Yoko organization: Kumamoto University – sequence: 3 givenname: Takatsugu orcidid: 0000-0003-1852-1835 surname: Ishimoto fullname: Ishimoto, Takatsugu organization: Kumamoto University – sequence: 4 givenname: Kosuke surname: Mima fullname: Mima, Kosuke organization: Kumamoto University – sequence: 5 givenname: Yukiharu surname: Hiyoshi fullname: Hiyoshi, Yukiharu organization: Kumamoto University – sequence: 6 givenname: Masaaki surname: Iwatsuki fullname: Iwatsuki, Masaaki organization: Kumamoto University – sequence: 7 givenname: Yoshifumi surname: Baba fullname: Baba, Yoshifumi organization: Kumamoto University – sequence: 8 givenname: Yuji surname: Miyamoto fullname: Miyamoto, Yuji organization: Kumamoto University – sequence: 9 givenname: Naoya surname: Yoshida fullname: Yoshida, Naoya organization: Kumamoto University – sequence: 10 givenname: Hideo orcidid: 0000-0002-3474-2550 surname: Baba fullname: Baba, Hideo email: hdobaba@kumamoto-u.ac.jp organization: Kumamoto University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30861255$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | 2019 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. 2019 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. 2019. This work is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| Snippet | Glucose transporter 1 (GLUT1) expression is a prognostic marker for esophageal squamous cell carcinoma (ESCC). Recent work on GLUT1 and development of specific... Glucose transporter 1 ( GLUT 1) expression is a prognostic marker for esophageal squamous cell carcinoma ( ESCC ). Recent work on GLUT 1 and development of... |
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| SubjectTerms | BAY‐876 Biomarkers Biopsy Cancer therapies Cell growth Cell Line, Tumor Cell proliferation Cell Proliferation - drug effects Chemotherapy Cisplatin Cisplatin - pharmacology Cisplatin - therapeutic use Deoxyglucose Deoxyribonucleic acid DNA DNA damage Drug Resistance, Neoplasm - drug effects Esophageal cancer Esophageal Neoplasms - drug therapy Esophageal Neoplasms - genetics Esophageal Neoplasms - metabolism Esophageal Neoplasms - surgery Esophageal Squamous Cell Carcinoma - drug therapy Esophageal Squamous Cell Carcinoma - genetics Esophageal Squamous Cell Carcinoma - metabolism Esophageal Squamous Cell Carcinoma - surgery Esophagus Extracellular signal-regulated kinase Female Gene Expression Regulation, Neoplastic - drug effects Glucose transporter Glucose Transporter Type 1 - genetics Glucose Transporter Type 1 - metabolism GLUT1 GLUT1 inhibitor Humans Immunohistochemistry L-Lactate dehydrogenase Lactic acid Male Medical prognosis Metabolism Original PET Pyrazoles - pharmacology Pyruvate kinase Pyruvic acid Quinolines - pharmacology RNA, Small Interfering - pharmacology Signal Transduction - drug effects siRNA Squamous cell carcinoma Surgery Tumors Western blotting |
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| Title | Glucose transporter 1 regulates the proliferation and cisplatin sensitivity of esophageal cancer |
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