TBK1 Facilitates GLUT1-Dependent Glucose Consumption by suppressing mTORC1 Signaling in Colorectal Cancer Progression Article Swipe
Diyuan Zhou
,
Yizhou Yao
,
Liang Zong
,
Guoqiang Zhou
,
Min Feng
,
Junjie Chen
,
Ganggang Liu
,
Guoliang Chen
,
Kang Sun
,
Huihui Yao
,
Yu Liu
,
Xinyu Shi
,
Weigang Zhang
,
Bo Shi
,
Qingliang Tai
,
Guanting Wu
,
Liang Sun
,
Wenqing Hu
,
Xinguo Zhu
,
Songbing He
·
YOU?
·
· 2022
· Open Access
·
· DOI: https://doi.org/10.7150/ijbs.70742
YOU?
·
· 2022
· Open Access
·
· DOI: https://doi.org/10.7150/ijbs.70742
Intestinal inflammation is a vital precipitating factor of colorectal cancer (CRC), but the underlying mechanisms are still elusive. TANK-binding kinase 1 (TBK1) is a core enzyme downstream of several inflammatory signals. Recent studies brought the impacts of TBK1 in malignant disease to the forefront, we found aberrant TBK1 expression in CRC is correlated with CRC progression. TBK1 inhibition impaired CRC cell proliferation, migration, drug resistance and tumor growth. Bioinformatic analysis and experiments in vitro showed overexpressed TBK1 inhibited mTORC1 signaling activation in CRC along with elevated GLUT1 expression without inducing GLUT1 translation. TBK1 mediated mTORC1 inhibition induces intracellular autophagy, which in turn decreasing GLUT1 degradation. As a rescue, blocking of autophagosome and retromer respectively via autophagy-related gene 7 (ATG7) or TBC1 Domain Family Member 5 (TBC1D5) silence diminished the regulation of TBK1 to GLUT1. GLUT1 staining presented that TBK1 facilitated GLUT1 membrane translocation which subsequently enhanced glucose consumption. Inhibitor of TBK1 also decreased GLUT1 expression which potentiated drug-sensitivity of CRC cell. Collectively, TBK1 facilitates glucose consumption for supporting CRC progression via initiating mTORC1 inhibition induced autophagy which decreases GLUT1 degradation and increases GLUT1 membrane location. The adaptive signaling cascade between TBK1 and GLUT1 proposes a new strategy for CRC therapy.
Related Topics
Concepts
TANK-binding kinase 1
mTORC1
GLUT1
Cancer research
Autophagy
Signal transduction
Biology
Cell biology
Glucose uptake
Endocrinology
MAPK/ERK pathway
Biochemistry
PI3K/AKT/mTOR pathway
Apoptosis
Insulin
MAP kinase kinase kinase
Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.7150/ijbs.70742
- https://www.ijbs.com/v18p3374.pdf
- OA Status
- gold
- Cited By
- 17
- References
- 45
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4285293470
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4285293470Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.7150/ijbs.70742Digital Object Identifier
- Title
-
TBK1 Facilitates GLUT1-Dependent Glucose Consumption by suppressing mTORC1 Signaling in Colorectal Cancer ProgressionWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2022Year of publication
- Publication date
-
2022-01-01Full publication date if available
- Authors
-
Diyuan Zhou, Yizhou Yao, Liang Zong, Guoqiang Zhou, Min Feng, Junjie Chen, Ganggang Liu, Guoliang Chen, Kang Sun, Huihui Yao, Yu Liu, Xinyu Shi, Weigang Zhang, Bo Shi, Qingliang Tai, Guanting Wu, Liang Sun, Wenqing Hu, Xinguo Zhu, Songbing HeList of authors in order
- Landing page
-
https://doi.org/10.7150/ijbs.70742Publisher landing page
- PDF URL
-
https://www.ijbs.com/v18p3374.pdfDirect link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
-
https://www.ijbs.com/v18p3374.pdfDirect OA link when available
- Concepts
-
TANK-binding kinase 1, mTORC1, GLUT1, Cancer research, Autophagy, Signal transduction, Biology, Cell biology, Glucose uptake, Endocrinology, MAPK/ERK pathway, Biochemistry, PI3K/AKT/mTOR pathway, Apoptosis, Insulin, MAP kinase kinase kinaseTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
17Total citation count in OpenAlex
- Citations by year (recent)
-
2025: 5, 2024: 4, 2023: 8Per-year citation counts (last 5 years)
- References (count)
-
45Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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