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The MYB-related Transcription Factor MYPOP acts as a Selective Regulator of Cancer Cell Growth

ABSTRACT: The MYB-related transcription factor and partner of profilin (MYPOP or p42POP) is a ubiquitously expressed and understudied protein, recently discovered in restricting oncogenic human papillomaviruses (HPV) and suggested as a tumor suppressor. In this study, we investigate the role of MYPOP on cancer cells. At supra-physiological levels, induced by both plasmid DNA- and messenger RNA-mediated gene transfer, MYPOP emerges as a potent tumor growth inhibitor, capable of inducing cancer cell death while sparing normal cells. Using HPV-transformed cervical cancer cells and normal human epidermal keratinocytes, cell behavior assessments as well as transcriptome analysis revealed MYPOP's specific anti-proliferative and death-inducing impact on cancer cells. We found MYPOP capable of silencing viral and human oncogenes including E6, E7, and MYC, and of triggering the release of the cancer-killing cytokine interleukin-24. Extending our research to murine Mypop, we observed anti-proliferative effects in mouse melanoma and colorectal cancer cells. Collectively, our findings underscore MYPOP's potential as a selective tumor suppressor in both human and mouse cancer cells, opening a promising avenue for future in vivo studies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE260896 | GEO | 2026/05/18

REPOSITORIES: GEO

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Project description:Head and neck cancer (HNC) is the fifth most common malignancy worldwide with an annual mortality rate of 200,000. About 90% of HNC can be classified as head and neck squamous cell carcinomas (HNSCC), of which approximately 75% are attributed to alcohol and tobacco consumption and 25 are associated with human papillomavirus (HPV), predominantly HPV16. HPV-associated OPC have better prognosis and a more favorable response to therapy as compared to HPV-negative tumors. Viral oncoproteins are capable of transforming primary human keratinocytes from either genital or oral epithelia in vitro and most likely play the same role in vivo, by disrupting cell-cycle regulatory pathways leading to a genetic progression to ano-genital cancer and OPC. However, the precise mechanisms by which HPV mediates malignant transformation of keratinocytes in the upper digestive tract epithelia are not entirely clear. HPV E7-mediated inactivation of pRb results in overexpression of p16INK4A, which is commonly used as a clinical surrogate marker for HPV positivity/activity. However, high p16INK4A alone has insufficient sensitivity and specificity as a biomarker of HPV positivity in different mucosal sub-sites of HNC. Therefore, increasing emphasis is being placed on the assessment of viral load and E7 oncogene expression, resulting in further classification of HPV positive OPC as HPV-active and HPV-inactive. Differences in risk factors, age of presentation, clinical behavior and gene expression profiles indicate that HPV-positive and HPV-negative tumors develop via different molecular mechanisms and are biologically distinct. This study aimed to compare the gene expression profiles of HPV-active OPCs and normal benign uvula/tonsil tissues and determine what biological processes and pathways are affected in HPV-active tumors. ANALYSIS 5: Two-condition, one-color experiment: HPV-active oropharyngeal tumor samples and normal benign uvula/tonsil tissues. Biological replicates: 12 HPV active samples and 4 Normal samples.

Project description:Head and neck cancer (HNC) is the fifth most common malignancy worldwide with an annual mortality rate of 200,000. About 90% of HNC can be classified as head and neck squamous cell carcinomas (HNSCC), of which approximately 75% are attributed to alcohol and tobacco consumption and 25 are associated with human papillomavirus (HPV), predominantly HPV16. HPV-associated OPC have better prognosis and a more favorable response to therapy as compared to HPV-negative tumors. Viral oncoproteins are capable of transforming primary human keratinocytes from either genital or oral epithelia in vitro and most likely play the same role in vivo, by disrupting cell-cycle regulatory pathways leading to a genetic progression to ano-genital cancer and OPC. However, the precise mechanisms by which HPV mediates malignant transformation of keratinocytes in the upper digestive tract epithelia are not entirely clear. HPV E7-mediated inactivation of pRb results in overexpression of p16INK4A, which is commonly used as a clinical surrogate marker for HPV positivity/activity. However, high p16INK4A alone has insufficient sensitivity and specificity as a biomarker of HPV positivity in different mucosal sub-sites of HNC. Therefore, increasing emphasis is being placed on the assessment of viral load and E7 oncogene expression, resulting in further classification of HPV positive OPC as HPV-active and HPV-inactive. Differences in risk factors, age of presentation, clinical behavior and gene expression profiles indicate that HPV-positive and HPV-negative tumors develop via different molecular mechanisms and are biologically distinct. This study aimed to compare the gene expression profiles of HPV-negative and HPV-inactive OPCs from both African American and European American patients, and determine their biological and racial differences. ANALYSIS 4: Four-condition, one-color experiment: African American (AA) HPV-inactive, African American (AA) HPV-negative, European American (EA) HPV-inactive, European American (EA) HPV-negative oropharyngeal tumor samples. Biological replicates: 4 AA HPV Inactive samples, 8 AA HPV Negative samples, 4 EA HPV Inactive samples and 8 EA HPV Negative samples,

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The MYB-related Transcription Factor MYPOP acts as a Selective Regulator of Cancer Cell Growth

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