Browsing by Subject "Cancer progression"

Now showing 1 - 3 of 3
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    Beyond an oncogene, Lin28 is a master regulator of cancer progression
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Wang, Xuefei; Weng, Mingjiao; Jin, Yinji; Yang, Weiwei; Wang, Xin; Wu, Di; Wang, Tianzhen; Li, Xiaobo
    The RNA binding protein Lin28 is increased in most human malignancies, and elevated Lin28 is a biomarker for poor prognosis and contributes to cancer progression. Lin28 functions as a master oncogene and is involved in almost all hallmarks of cancer. In this review, we summarize the aberrant molecular expression mechanisms and pathological roles of Lin28 in cancer progression. Moreover, we elaborate on the established molecular mechanisms, from the transcriptional level to the post-transcriptional and translational levels, by which Lin28 regulates cancer progression.
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    Open Access
    Circular RNAs: Characteristics, function and role in human cancer
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Chen, Shuo; Zhao, Yang
    Circular RNAs (circRNAs) are universal and diverse endogenous noncoding RNAs (ncRNAs) that are widely found in eukaryotic cells. They form a covalently closed, continuous stable loop structure without 3' or 5' tails, which are different from linear RNAs. As new members of the ncRNAs, circRNAs’ formation, function, and mechanism are attracting increased research attention. CircRNAs play important roles in all kinds of cancer and may be potential novel biomarkers and therapeutic targets for cancer treatment through their function as microRNA (miRNA) molecular “sponges”, RNA-binding protein (RBP) sponges, protein translators, and gene transcription regulators. In this review, we introduce the formation and function of circRNAs, and summarize the biological effects of circRNA in tumorigenesis and progression, providing evidence for the potential use of circRNAs in the diagnosis and clinical treatment of cancer.
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    Open Access
    Differential expression of ferroptosis markers, circadian regulators, KLOTHO, and classical tumor suppressors in colorectal cancer according to tumor stage: Influence of age, anatomical location, and correlation patterns
    (2025) Cielo Garcia Montero; Oscar Fraile Martinez; Ana M. Minaya Bravo; Diego Liviu Boaru; Diego De Leon Oliva; Patricia De Castro Martinez; Majd N. Michael Alhaddadin; Silvestra Barrena Blázquez; Laura Lopez Gonzalez; Luis G. Guijarro; Natalio Garcia Honduvilla; Víctor Roberto Baena Romero; Carlos Daniel Padilla Ansala; Mar Royuela; María Del Val Toledo Lobo; Leonel Pekarek; Roberto Fernández Baillo Gallego de la Sacristana; Mauricio Hernández Fernández; Montserrat Chao Crecente; Melchor Alvarez-Mon; Raul Diaz-Pedrero; Miguel A. Ortega; Miguel A. Saez; Biología Celular e Histología
    Colorectal cancer (CRC) is a leading cause of cancer-related mortality, with an incidence projected to rise significantly worldwide. While TNM staging remains the cornerstone of prognosis and treatment decisions, additional biomarkers are needed to enhance predictive accuracy and therapeutic targeting. Ferroptosis, an iron-dependent cell death pathway, has emerged as a key regulator of CRC progression and therapy resistance. Circadian rhythms, KLOTHO, and tumor suppressors, such as p53, CDKN1A (p21), and Rb, also play crucial roles in CRC biology. Integrating TNM staging with molecular markers and patient-specific variables offers a more precise, personalized approach to CRC management. In the present work, we analyze the histopathological expression of KLOTHO, ferroptosis markers (TFRC, ALOX-5, ACSL-4, and GPX-4), circadian regulators (CLOCK, BMAL1, PER1, and PER2), and classical tumor suppressors (p53, p21, and Rb) in a cohort of 63 patients diagnosed with CRC. Besides, we have considered important clinical variables, like sex, age, and anatomical location, in our statistical analysis; correlation with the protein expression of these markers was also included for each stage (T1, T2, and T3). Our study reveals that advanced CRC stages (primarily T3) exhibit increased expression of ferroptosis markers (TFRC, ALOX5, ACSL4, and GPX4) and tumor suppressors (p53, p21, and Rb), alongside reduced histopathological detection of KLOTHO and circadian markers (BMAL1, CLOCK, PER1, and PER2) compared with earlier stages. Age, but not sex, influenced the expression of several markers. Tumor location also played a role, with right-sided CRCs showing significant stage-related differences in ferroptosis, tumor suppressor, and BMAL1, whereas left-sided tumors exhibited variations primarily in circadian markers (CLOCK, PER1, and PER2). Correlation analyses across tumor stages indicate dynamic shifts, with tumor suppressors maintaining positive associations with ferroptosis markers and anti-aging/circadian markers showing stage-dependent changes. Despite the inherent limitations of our study, these findings highlight the evolving biomarker landscape in CRC progression, although further research is needed to elucidate their clinical implications.