LMLucero Martínez-Retamoza

Lucero Martínez-Retamoza

*This is an algorithmically generated author record based on publicly available information.

Current Organizations / Institutes

The organizations/institutes from the scholar's latest article


Lucero Martínez-Retamoza has a total of 8 co-authors. Here are the top co-authors by number of shared publications:


Latest Publications

  • Open Access

    miRNAs Dysregulated in Human Papillomavirus-Associated Benign Prostatic Lesions and Prostate Cancer

    by Sandra Viridiana Salgado-Hernández, Lucero Martínez-Retamoza, Rodolfo Ocadiz-Delgado, Salvador Pérez-Mora, Gladys Edith Cedeño-Arboleda, María del Consuelo Gómez-García, Patricio Gariglio, 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


  • Open Access

    Dysregulated Expression of Selected miRNAs in Human Papillomavirus-Positive Patients with Benign Prostatic Hyperplasia/Prostatitis and Prostate Cancer

    by Sandra Viridiana Salgado-Hernández, Lucero Martínez-Retamoza, Rodolfo Ocadiz-Delgado, Salvador Pérez-Mora, Gladys Cedeño-Arboleda, María del Consuelo Gómez-García, Patricio Gariglio, 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.