Lucero Isabel Martinez-Retamoza

Dr. Lucero Isabel Martinez-Retamoza

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Research Focus & Metrics

Academic Career Length

3Years (2024-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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25 December 2024 in Cancers
Verified
Journal Article
Open access
PDF file
SHSandra Viridiana Salgado Hernandez
Sandra Viridiana Salgado Hernandez
LMLucero Isabel Martinez-Retamoza
Lucero Isabel Martinez-Retamoza
RDRodolfo Ocadiz Delgado
Rodolfo Ocadiz Delgado
Salvador PérezSalvador Pérez
Salvador Pérez
GCGladys Edith Cedeño-Arboleda
Gladys Edith Cedeño-Arboleda
David Guillermo Pérez-IshiwaraDavid Guillermo Pérez-Ishiwara
David Guillermo Pérez-Ishiwara
Prostate pathologies, including chronic prostatitis, benign prostatic hyperplasia (BPH), and prostate cancer (PCa), are strongly associated with chronic inflammation, which is a key risk factor and hallmark of these diseases

16 September 2024 in Preprints.org
Verified
Preprint
Open access
PDF file
SHSandra Viridiana Salgado Hernandez
Sandra Viridiana Salgado Hernandez
LMLucero Isabel Martinez-Retamoza
Lucero Isabel Martinez-Retamoza
RDRodolfo Ocadiz Delgado
Rodolfo Ocadiz Delgado
SPSalvador Pérez-Mora
Salvador Pérez-Mora
GCGladys Cedeño-Arboleda
Gladys Cedeño-Arboleda
David Guillermo Pérez-IshiwaraDavid Guillermo Pérez-Ishiwara
David Guillermo Pérez-Ishiwara
Chronic prostatitis has been found to be associated with the genesis of Benign Prostatic Hyper-plasia (BPH) and subsequent development of prostate cancer (PCa). It has been described that human papillomavirus (HPV) tends to infect the prostatic epithelium; however, correlation be-tween HPV infection and prostate pathology remains to be elucidated. Considering that HPV in-fection can affect cellular pathways, we investigated here the putative role of HPV in the expres-sion of selected miRNAs involved in inflammation, proliferation, and oncogenesis in BPH, BPH/prostatitis and PCa clinical samples. Our results demonstrated that 67.2 % of benign lesions and 93.4% of cancer samples were HPV-positive. Interestingly, we found downregulation of miR-34a, miR-143, and miR-145, as well as upregulation of miR-221 in tissue with BPH and BPH/prostatitis. In HPV-positive PCa samples, let-7c, miR-34a, miR-126, miR-221, miR-145, and miR-106a were found to be downregulated, suggesting their involvement in the formation of a pro-oncogenic microenvironment. Consistent with these results, we found that altered expression levels of miR-34a, miR-145, miR-106a, miR-21 and miR-221 showed a correlation with high-risk HPV-positive PCa samples. The differential expression of these miRNAs induced by HPV could be useful for the identification of potential therapeutic biomarkers, opening a new approach for di-agnosis, prognosis, and therapeutic targeting in prostate cancer.