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Research Article
Christian R. Gomez
University of Mississippi Medical Center
Corresponding Author
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Background: The major histocompatibility complex class I polypeptide-related sequence A gene (MICA) is one of the ligands of NKG2D activating receptor. MICA stimulates NKG2D that further triggers activation of natural killer cells which leads to killing of infected target cells. Tumor cells utilize escape strategies to subvert the biological function of NKG2D by shedding overexpressing MICA. In this study, we determine the levels of MICA colorectal cancers (CRCs). Additionally, we establish correlations between MICA expression and clinical characteristics. Publicly available data and bioinformatics tools are used for validation purposes.
Methods: We determined the MICA RNA expression levels and correlation with clinicopathological parameters in CRC using UALCAN web-portal. We performed immunohistochemical analysis on tissue microarrays having 192 samples, acquired from 96 CRC patients to validate the expression of MICA in CRC and adjacent uninvolved tissue and investigated its prognostic significance by Kaplan-Meir and proportional hazards methods.
Results: Bioinformatics and immunohistochemical analyses showed that MICA expression was significantly upregulated in CRCs as compared to uninvolved and the overexpression of MICA was independent of pathologic stage, histotype, nodal metastasis status, p53-status, as well as patient’s race, age and gender. Moreover, PROGgeneV2 survival analysis of two cohorts showed poor prognosis of CRC patients exhibiting high MICA expression.
Conclusions: Overall, our findings demonstrate high expression of MICA, suggest poor prognosis of CRC patients exhibiting high MICA expression. These results can be further explored due to its potential to provide clues to the mechanistic contributing role of the tumor microenvironment to the progression of progression of CRC.
Keywords
MICA, IHC, colorectal cancer, expression, prognostic marker
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No competing interests reported.
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This preprint is under consideration at BMC Cancer. A preprint is 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
Christian R. Gomez
University of Mississippi Medical Center
Corresponding Author
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: Under Review
Version 1
Posted 22 Mar, 2021
No community comments so far
Reviewers invited
Invitations sent on 28 Mar, 2021
Editor assigned
On 28 Mar, 2021
Editor invited
On 17 Mar, 2021
Submission checks complete
On 16 Mar, 2021
First submitted
On 09 Mar, 2021
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cancer Biology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: The major histocompatibility complex class I polypeptide-related sequence A gene (MICA) is one of the ligands of NKG2D activating receptor. MICA stimulates NKG2D that further triggers activation of natural killer cells which leads to killing of infected target cells. Tumor cells utilize escape strategies to subvert the biological function of NKG2D by shedding overexpressing MICA. In this study, we determine the levels of MICA colorectal cancers (CRCs). Additionally, we establish correlations between MICA expression and clinical characteristics. Publicly available data and bioinformatics tools are used for validation purposes.
Methods: We determined the MICA RNA expression levels and correlation with clinicopathological parameters in CRC using UALCAN web-portal. We performed immunohistochemical analysis on tissue microarrays having 192 samples, acquired from 96 CRC patients to validate the expression of MICA in CRC and adjacent uninvolved tissue and investigated its prognostic significance by Kaplan-Meir and proportional hazards methods.
Results: Bioinformatics and immunohistochemical analyses showed that MICA expression was significantly upregulated in CRCs as compared to uninvolved and the overexpression of MICA was independent of pathologic stage, histotype, nodal metastasis status, p53-status, as well as patient’s race, age and gender. Moreover, PROGgeneV2 survival analysis of two cohorts showed poor prognosis of CRC patients exhibiting high MICA expression.
Conclusions: Overall, our findings demonstrate high expression of MICA, suggest poor prognosis of CRC patients exhibiting high MICA expression. These results can be further explored due to its potential to provide clues to the mechanistic contributing role of the tumor microenvironment to the progression of progression of CRC.
Figure 1
Figure 2
Figure 3
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