See the published version of this preprint at Molecular Medicine.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research article
Yanhui Liu
Sichuan University West China Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0002-3722-3334
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Malignant glioma exerts a metabolic shift from oxidative phosphorylation (OXPHOs) to aerobic glycolysis, with suppressed mitochondrial functions. This phenomenon offers a proliferation advantage to tumor cells and decrease mitochondria-dependent cell death. However, the underlying mechanism for mitochondrial dysfunction in glioma is not well elucidated. MTCH2 is a mitochondrial outer membrane protein that regulates mitochondrial metabolism and related cell death. This study aims to clarify the role of MTCH2 in glioma.
Methods: Bioinformatic analysis from TCGA and CGGA databases were used to investigate the association of MTCH2 with glioma malignancy and clinical significance. The expression of MTCH2 was verified from clinical specimens using real-time PCR and western blots in our cohorts. siRNA-mediated MTCH2 knockdown were used to assess the biological functions of MTCH2 in glioma progression, including cell invasion and temozolomide-induced cell death. Biochemical investigations of mitochondrial and cellular signaling alternations were performed to detect the mechanism by which MTCH2 regulates glioma malignancy.
Results: Bioinformatic data from public database and our cohort showed that MTCH2 expression was closely associated with glioma malignancy and poor patient survival. Silencing of MTCH2 expression impaired cell migration/invasion and enhanced temozolomide sensitivity of human glioma cells. Mechanistically, MTCH2 knockdown may increase mitochondrial OXPHOs and thus oxidative damage, decreased migration/invasion pathways, and repressed pro-survival AKT signaling.
Conclusion: Our work establishes the relationship between MTCH2 expression and glioma malignancy, and provides a potential target for future interventions.
Keywords
MTCH2, glioma, temozolomide, mitochondria, cell migration/invasion, cell death
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
This is a list of supplementary files associated with this preprint. Click to download.
Loading...
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at Molecular Medicine.
Version 3
Posted 31 Dec, 2020
No community comments so far
Reviewers invited
Invitations sent on 16 Dec, 2020
Reviewer #1 agreed
On 16 Dec, 2020
Review #1 received
Received 16 Dec, 2020
Editorial decision: Accept
On 16 Dec, 2020
Editor assigned
On 10 Dec, 2020
Submission checks complete
On 10 Dec, 2020
Editor invited
On 10 Dec, 2020
No comments provided
Reviewer #2 agreed
On 25 Nov, 2020
Review #2 received
Received 25 Nov, 2020
Reviewers invited
Invitations sent on 23 Nov, 2020
Reviewer #1 agreed
On 23 Nov, 2020
Editor assigned
On 17 Nov, 2020
Submission checks complete
On 17 Nov, 2020
Editor invited
On 17 Nov, 2020
No comments provided
Editorial decision: Major revision
On 09 Sep, 2020
Review #2 received
Received 29 Aug, 2020
Review #1 received
Received 16 Aug, 2020
Reviewer #3 agreed
On 12 Aug, 2020
Reviewer #1 agreed
On 11 Aug, 2020
Reviewer #2 agreed
On 11 Aug, 2020
Editor assigned
On 10 Aug, 2020
Reviewers invited
Invitations sent on 10 Aug, 2020
Editor invited
On 09 Aug, 2020
Submission checks complete
On 06 Aug, 2020
First submitted
On 03 Aug, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Laboratory Diagnostics
Learn more about our company.
See the published version of this preprint at Molecular Medicine.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research article
Yanhui Liu
Sichuan University West China Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0002-3722-3334
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at Molecular Medicine.
Version 3
Posted 31 Dec, 2020
No community comments so far
Reviewers invited
Invitations sent on 16 Dec, 2020
Reviewer #1 agreed
On 16 Dec, 2020
Review #1 received
Received 16 Dec, 2020
Editorial decision: Accept
On 16 Dec, 2020
Editor assigned
On 10 Dec, 2020
Submission checks complete
On 10 Dec, 2020
Editor invited
On 10 Dec, 2020
No comments provided
Reviewer #2 agreed
On 25 Nov, 2020
Review #2 received
Received 25 Nov, 2020
Reviewers invited
Invitations sent on 23 Nov, 2020
Reviewer #1 agreed
On 23 Nov, 2020
Editor assigned
On 17 Nov, 2020
Submission checks complete
On 17 Nov, 2020
Editor invited
On 17 Nov, 2020
No comments provided
Editorial decision: Major revision
On 09 Sep, 2020
Review #2 received
Received 29 Aug, 2020
Review #1 received
Received 16 Aug, 2020
Reviewer #3 agreed
On 12 Aug, 2020
Reviewer #1 agreed
On 11 Aug, 2020
Reviewer #2 agreed
On 11 Aug, 2020
Editor assigned
On 10 Aug, 2020
Reviewers invited
Invitations sent on 10 Aug, 2020
Editor invited
On 09 Aug, 2020
Submission checks complete
On 06 Aug, 2020
First submitted
On 03 Aug, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Laboratory Diagnostics
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at Molecular Medicine.
Background: Malignant glioma exerts a metabolic shift from oxidative phosphorylation (OXPHOs) to aerobic glycolysis, with suppressed mitochondrial functions. This phenomenon offers a proliferation advantage to tumor cells and decrease mitochondria-dependent cell death. However, the underlying mechanism for mitochondrial dysfunction in glioma is not well elucidated. MTCH2 is a mitochondrial outer membrane protein that regulates mitochondrial metabolism and related cell death. This study aims to clarify the role of MTCH2 in glioma.
Methods: Bioinformatic analysis from TCGA and CGGA databases were used to investigate the association of MTCH2 with glioma malignancy and clinical significance. The expression of MTCH2 was verified from clinical specimens using real-time PCR and western blots in our cohorts. siRNA-mediated MTCH2 knockdown were used to assess the biological functions of MTCH2 in glioma progression, including cell invasion and temozolomide-induced cell death. Biochemical investigations of mitochondrial and cellular signaling alternations were performed to detect the mechanism by which MTCH2 regulates glioma malignancy.
Results: Bioinformatic data from public database and our cohort showed that MTCH2 expression was closely associated with glioma malignancy and poor patient survival. Silencing of MTCH2 expression impaired cell migration/invasion and enhanced temozolomide sensitivity of human glioma cells. Mechanistically, MTCH2 knockdown may increase mitochondrial OXPHOs and thus oxidative damage, decreased migration/invasion pathways, and repressed pro-survival AKT signaling.
Conclusion: Our work establishes the relationship between MTCH2 expression and glioma malignancy, and provides a potential target for future interventions.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
This is a list of supplementary files associated with this preprint. Click to download.
Loading...