DigitalUM :: Browsing by Subject "Oncogene"

Browsing by Subject "Oncogene"

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Open Access
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.
Open Access
lmmunoreactivity for c-fos and c-myc protein with the monoclonal antibodies 14E10 and 6E10 in malignant mesothelioma and nonneoplastic mesothelium of the pleura
(Murcia : F. Hernández, 1995) Ramael, M.; Van den Bossche, J.; Buysse, C.; Deblier, I.; Segers, K.; Van Marck, E.
We studied immunoreactivity for c-fos protein and c-myc protein in malignant mesothelioma (36 cases) and non-neoplastic pleural mesothelium (45 cases) using the murine monoclonal antibodies 14E10 and 6E10. All malignant mesotheliomas and cases with non-neoplastic mesothelium exhibited not only nuclear but also cytoplasmic immunoreactivity for c-fos and cmyc protein in the majority of mesothelial cells. There was no statistically significant difference between the various mesothelioma subtypes or between neoplastic and non-neoplastic mesothelium for c-fos protein immunoreactivity (p>0.05). There was statistically significant difference between neoplastic and nonneoplastic mesothelium for c-myc protein immunoreactivity (p<0.0 1). We conclude that immunoreactivity for c-fos and cmyc protein is present in both non-neoplastic and neoplastic mesothelium, but that a higher proportion of neoplastic mesothelial cells are immunoreactive for cmyc protein when compared with non-neoplastic mesothelium.
Open Access
MiR-503-5p functions as an oncogene in oral squamous cell carcinoma by targeting Smad7
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Fei, Yifan; Shan, Weilan; Chen, Xiaoqing
Background. Oral squamous cell carcinoma (OSCC) is a common oral malignancy. Previous studies indicated that the level of miR-503-5p was upregulated in OSCC tissues. However, the mechanism by which miR-503-5p regulates the proliferation and invasion of OSCC cells remains unclear. Therefore, this study aimed to investigate the role of miR-503-5p during the progression of OSCC. Methods. The level of miR-503- 5p in Tca8113 cells was detected using RT-qPCR assay. In addition, CCK-8, transwell assays and flow cytometry assays were conducted to detect cell viability, migration, invasion and apoptosis, respectively. Meanwhile, the dual luciferase reporter assay was applied to explore the interaction between miR-503-5p and Smad7 in Tca8113 cells. Results. Overexpression of miR-503-5p significantly promoted the proliferation, migration and invasion of Tca8113 cells, while downregulation of miR- 503-5p markedly inhibited proliferation, migration and invasion of cells. In addition, knockdown of miR-503-5p obviously induced the apoptosis of Tca8113 cells via increasing the levels of Bax and cleaved caspase 3, and decreased the expression of Bcl-2. Moreover, SMAD family member 7 (Smad7) was identified as a direct binding target of miR-503-5p in Tca8113 cells. Overexpression of miR-503-5p significantly downregulated the levels of Smad7 and E-cadherin, but upregulated the levels of N-cadherin and MMP-9 in Tca8113 cells. Conclusion. These results indicated that miR-503-5p might act as an oncogene in OSCC cells by targeting Smad7. Therefore, miR-503-5p might act as a novel and potential therapeutic target for the treatment of OSCC
Open Access
MlBl proliferation index in breast infiltrating carcinoma: Comparison with other proliferative markers and association with new biological prognostic factors
(Murcia : F. Hernández, 2001) González-Vela, M.C.; Garijo, M.F.; Fernández, F.; Val-Bernal, José Fernando
Aims: In breast invasive carcinoma our objectives were 1) to compare cellular proliferation determined by MIBl index with S-phase fraction (SPF) assessed by flow cytometry and with mitotic index, and 11) to examine the association of MIBl index with classical and with new biological prognostic factors [bcl- 2, p53, c-erbB-2 and cathepsin D (CD)]. Methods and results: From 102 cases of breast invasive carcinoma, 5- pm thick serial sections were cut from formalin-fixed, paraffin-embedded tissue blocks, and processed for detection of CD, c-erbB-2, p53, bcl-2, Ki-67 antigen MIB-1 and estrogen receptors (ER) and progesterone receptors (PR). SPF was measured by flow cytometry in fresh-frozen tissue samples taken from the carcinoma in each patient. MIBl index was correlated with SPF (rho=0.45, pe0.0001) and with mitotic index (rho=0.42, p<0.0001). The MIB-1 index was positively associated with the histological grade (p=0.001), tumor size (p=0.04) and the presence of metastases in axillary lymph nodes (p=0.01). MIBl was associated directly with p53 @=0.045) and inversely with bcl-2 @=0.0002). The MIB-1 index was not statistically associated with cerbB- 2. There was a weak association between MIBl index and stromal cell CD. The median MIBl index was higher in tumors with moderate to strong CD staining of stromai cell, but the difference did not reach statistical significance (p=0.09). Conclusions: MIBl index correlates with well established methods for assessing tumor proliferation and with parameters of an aggressive phenotype of tumor. MIBl index is an effective and readily accessible method for assessing tumor proliferation in breast carcinoma.
Open Access
Molecular pathology of low malignant bladder transitional cell carcinoma: a current perspective
(Murcia : F. Hernández, 2005) Wang, H.T.; Chang, J.W.
Bladder transitional cell carcinoma (BTCC) actually has two phenotypes: low malignant and aggressive. Most previous molecular and cytogenetic analyses of bladder cancer were focused on aggressive BTCC. Little is known about the events that lead to the development of low malignant BTCC. This review mainly introduces the concept of two types of bladder tumors and then focuses on the molecular pathology of low malignant BTCC in particular. It is hoped that further understanding of the molecular pathology of low malignant BTCC may provide novel therapies and many other clinical benefits in patients with this disease.
Open Access
Notch1 in oral squamous cell carcinoma
(Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Yoshida, Ryoji; Ito, Takaaki; Abdo Hassan, Wael; Nakayama, Hideki
Notch signaling has been reported to be involved in several types of malignant tumors. However, the role and activation mechanisms of Notch signaling in oral squamous cell carcinoma (OSCC) remain poorly characterized. The present review focuses on the dual role of Notch signaling in OSCC. A number of expression and functional analyses demonstrated that Notch1 plays a crucial role in development and progression of OSCC. On the other hand, a tumor suppressive role of Notch1 was also suggested from studies, based on deep sequencing of cancer genomes. Interestingly, although some Notch1 mutations overlap in tumors from Caucasian and Asian patients, the overall spectrum of such mutations is vastly different between these cohorts. Accumulating evidence suggests that variation of Notch1 mutation signature may determine the role of Notch signaling in OSCC. As Notch is thought to act as an oncogene in a subset of OSCC, but also has a tumor suppression role, the role of Notch in OSCC seems to be highly context dependent.
Open Access
Novel oncogene HCCR: its diagnostic and therapeutic implications for cancer
(Murcia : F. Hernández, 2005) Chung, Y.J.; Kim, J.W.
Identification of robust diagnostic and therapeutic target molecules for human malignancy is still an important issue. If we identify novel proteins which play a stem-line role for cellular transformation or aggravation of malignancy, it could give us a clue to diagnose a tumor in an earlier stage and to develop more reliable therapeutic tools. For this purpose, we have screened abnormally expressed genes in various human cancers by differential display RT-PCR. One of the overexpressed genes was a human cervical cancer oncogene (HCCR). HCCR was not only identified in cervical cancer tissues, but also found to be overexpressed in various human malignancies such as leukemia/lymphoma, breast, kidney, stomach, colon, liver and ovarian cancer. This molecule appeared to be a negative regulator of p53. In this paper, we discuss the biological functions of HCCR molecules and its implications for early diagnosis and future development of therapeutic devices of cancer.
Open Access
Periostin acts as an oncogene to promote laryngeal cancer progression by activating decorin
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Wu, Chao; Yang, Bo; Chu, Jiusheng
Laryngeal carcinoma (LC) is the second most common malignancy of the head and neck worldwide, with increasing incidence every year. However, the mechanism of its development is not completely clear. Periostin (POSTN) has been reported to be involved in various aspects of tumorigenesis. To determine the influence of POSTN on LC tumorigenesis, we first examined the expression of POSTN in tissues from patients with LC through immunohistochemistry, western blot, and qRT-PCR. Besides, we demonstrated that POSTN promoted LC cell migration, invasion, and proliferation in vitro by CCK-8, colony formation, and Transwell assays, and tumor growth in vivo by immunohistochemistry. Furthermore, the interaction between POSTN and decorin (DCN) was further verified by bioinformatics analysis and immunoprecipitation (IP), finding that POSTN promoted the malignant progression of LC by targeting DCN. Our findings support the idea that the level of POSTN expression and accumulation in tumors correlated with the malignancy degree of LC, suggesting that POSTN may play a potential role in improving laryngeal cancer treatment strategies
Open Access
Ring finger protein 126: a potential biomarker for colorectal cancer
(2021) Huang, Chaoqun; Min, Yao; Liu, Jiuyang; Li, Jing; Yang, Xiaojun
Background. Colorectal cancer (CRC) is the most common cancer of the digestive system. However, effective therapeutic targets against CRC have not been found yet. Further, the relationship between the expression of ring finger protein 126 (RNF126) and CRC is not clear. Material and Methods. The expression level of RNF126 in CRC tissues and cell lines was detected by immunohistochemical staining and western blot. Subsequently, endogenous RNF126 expression was inhibited in a CRC cell line using a short hairpin RNA. Next, the effect of RNF126 on the properties of CRC cells was studied through different experimental methods. Results. We found that the RNF126 protein was mainly localized in the cytoplasm. High RNF126 expression was observed to be an independent risk factor for poor prognosis in CRC patients. In vitro studies showed that RNF126 was able to promote the proliferation, migration, and invasion ability of CRC cells. Conclusion. RNF126 acts as an oncogene during CRC development, and may serve as a novel target for CRC treatment.
Open Access
The transcription factor Fos, a Janus-type regulator in health and disease
(Murcia : F. Hernández, 2009) Durchdewald, Moritz; Angel, Peter; Hess, Jochen
The immediate early gene product Fos is part of the activator protein-1 (AP-1) transcription factor and has been shown to participate in the molecular mechanisms of cell proliferation, differentiation, apoptosis, and transformation. The analysis of genetically modified mice and cells derived thereof has provided important new insights into its specific biological functions in development, tissue homeostasis, and cellular responses to environmental insults. Moreover, the deregulation of Fos could be linked with a variety of pathological conditions, including immunological, skeletal and neurological defects, as well as oncogenic transformation and tumor progression. In contrast to the mainstream opinion concerning the oncogenic function of Fos an increasing number of experimental reports also describe a tumor-suppressive function in various cancer types. More recently, altered Fos expression in cell culture and mouse models combined with global gene expression analysis unraveled novel downstream effectors of the Fosregulated genetic program. Finally, selective inhibition of its function with a small molecule inhibitor in a preclinical mouse model of arthritis demonstrated that targeting Fos/AP-1 activity could be an auspicious new option for clinical use.

Browsing by Subject "Oncogene"

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