scholarly journals Loss of HOXB3 promotes development of hormone receptor negative breast cancer

2020 ◽  
Author(s):  
Lizhe Zhu ◽  
Shibo Yu ◽  
Siyuan Jiang ◽  
Guanqun Ge ◽  
Yu Yan ◽  
...  

Abstract BackgroundThe homobox (HOX) gene family as a transcription factor encoding a specific nuclear protein is essential for embryonic development, differentiation, and homeostasis. The role of HOXB3 protein varies in different tumors. This study aims to explore the role of the HOXB3 gene in breast cancer.MethodDifferentiated expressed genes were screened by analyzing metastatic breast cancer gene chip data in TCGA and GEO database. The function of selected HOXB3 gene was also analyzed by GEPIA, Kaplan-Meier Plotter, Breast Cancer Gene-Expression Miner and metascape. Molecular biology methods such as qRT-PCR, western blot and IF was used to verify bio-informatics findings.ResultsBoth bio-informatics analyses and western blot showed that HOXB3 was lost in breast cancer compared to normal breast tissue. Survival analysis also showed that lower expression of HOXB3 was associated with poor prognosis. Bio-informatics analyses further showed that HOXB3 was positively correlated with hormone receptors. qRT-PCR, immunofluorescence and western blot also confirmed that HOXB3 had the highest expression in the immortalized breast epithelial cell line MCF-10A, lower in luminal breast cancer cell line T47D and the lowest in triple negative breast cancer (TNBC) cell line MDA-MB-231. Metascape for GO analysis of GEO data provided possible mechanism that HOXB3 could positively regulate cell adhesion, inhibit cell proliferation and activate immune response in breast cancer, and considered that HOXB3 might cause cell malignant transformation through the above pathways.ConclusionIn summary, HOXB3 expression was decreased in breast cancer, especially in hormone receptor-negative breast cancer. The lower expression of HOXB3 was associated with poor prognosis. It might become a new biomarker to predict prognosis of breast cancer.

2020 ◽  
Vol 35 (2) ◽  
pp. 56-65
Author(s):  
Yang Chen ◽  
Jiameng Liu ◽  
Ningbo Geng ◽  
Chongjin Feng

Background: A well-known transcriptional regulator of the proto-oncogene c-Myc, far-upstream element (FUSE) binding protein 1 (FUBP1) has been demonstrated by previous work to be aberrantly expressed in lots of cancers and plays a critical role in tumor progression; however, its expression and function in tongue squamous cell carcinoma (TSCC) remains unclear. Methods: Evaluations with immunohistochemistry, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were performed to assess FUBP1 expression. The correlations of FUBP1 expression levels with various clinicopathological factors were evaluated with univariate and multivariate analyses. In addition, the role of FUBP1 in TSCC proliferation was studied in TSCC cells by silencing FUBP1. The role of FUBP1 on proliferation and apoptosis was confirmed by cell counting Kit-8, colony formation, cell cycle, and cell apoptosis assays. Results: Immunohistochemistry, qRT-PCR and Western blot results showed FUBP1 expression was higher in TSCC tissues in comparison with adjacent non-cancerous tissues ( P <0.05), as well as in patients with advanced-stage disease or cervical lymph node metastasis ( P<0.001). The 5-year survival rate was significantly lower in the group with high FUBP1 expression than in that with low FUBP1 expression ( P=0.035). FUBP1 expression was also an independent predictor for overall survival in TSCC patients, and was closely related to poor prognosis. FUBP1 knockdown inhibited cancer cell proliferation, and induced cell cycle arrest and apoptosis. Conclusion: FUBP1 was overexpressed in TSCC, and correlated with TSCC cell proliferation and poor prognosis. FUBP1 appears to act as a potential oncogene in TSCC, and may be considered a novel biomarker for TSCC.


Science News ◽  
1995 ◽  
Vol 148 (10) ◽  
pp. 149
Author(s):  
L. Seachrist

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e10421
Author(s):  
Lizhe Zhu ◽  
Shibo Yu ◽  
Siyuan Jiang ◽  
Guanqun Ge ◽  
Yu Yan ◽  
...  

Background The homeobox gene family, encoding a specific nuclear protein, is essential for embryonic development, differentiation, and homeostasis. The role of the HOXB3 protein varies in different tumors. This study aims to explore the role of the HOXB3 gene in breast cancer. Method Differentially expressed genes were screened by analyzing metastatic breast cancer gene chip data from TCGA and GEO databases. The function of the selected HOXB3 gene was also analyzed in different databases and through molecular biology methods, such as qRT-PCR, western blot and IF to verify bioinformatics findings. Results Both bioinformatics analyses and western blot showed that HOXB3 was lost in breast cancer compared to normal breast tissue. Survival analysis also showed that lower expression of HOXB3 was associated with poor prognosis. Bioinformatics analyses further showed that HOXB3 was positively correlated with hormone receptors. Metascape for GO analysis of GEO data provided possible mechanisms that HOXB3 could positively regulate cell adhesion, inhibit cell proliferation and activate immune response in breast cancer; moreover, GSEA included several cancer-associated pathways. Conclusion In summary, HOXB3 expression was decreased in breast cancer, and it was associated with poor prognosis. It might become a new biomarker to predict prognosis of breast cancer.


Cell Division ◽  
2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Yair Alfaro-Mora ◽  
Guadalupe Domínguez-Gómez ◽  
Rodrigo E. Cáceres-Gutiérrez ◽  
Laura Tolentino-García ◽  
Luis A. Herrera ◽  
...  

Abstract Background It has been reported that the oncoprotein E7 from human papillomavirus type 16 (HPV16-E7) can induce the excessive synthesis of centrosomes through the increase in the expression of PLK4, which is a transcriptional target of E2F1. On the other hand, it has been reported that increasing MPS1 protein stability can also generate an excessive synthesis of centrosomes. In this work, we analyzed the possible role of MPS1 in the amplification of centrosomes mediated by HPV16-E7. Results Employing qRT-PCR, Western Blot, and Immunofluorescence techniques, we found that E7 induces an increase in the MPS1 transcript and protein levels in the U2OS cell line, as well as protein stabilization. Besides, we observed that inhibiting the expression of MPS1 in E7 protein-expressing cells leads to a significant reduction in the number of centrosomes. Conclusions These results indicate that the presence of the MPS1 protein is necessary for E7 protein to increase the number of centrosomes, and possible implications are discussed.


2010 ◽  
Vol 01 (01) ◽  
pp. 26-31
Author(s):  
D. Gadzicki ◽  
M. Neises

ZusammenfassungDer Nachweis der Gene BRCA (breast cancer gene) 1 und 2 in den Jahren 1994 und 1995 war die Voraussetzung für die Diagnostik genetischer Grundlagen des familiären Mamma- und Ovarialkarzinoms. Eine Mutation in einem dieser Gene ist der wichtigste Risikofaktor für die Entstehung eines solchen Karzinoms. Etwa 5–10 % aller Mamma- und Ovarialkarzinome sind durch genetische Veranlagung bedingt. Die Möglichkeiten der prädiktiven Medizin können sowohl Entlastung, aber auch psychische Belastungen der Ratsuchenden nach sich ziehen. Die Kenntnis der eigenen Prognose oder die anderer innerhalb der Familie kann die Kommunikation und damit die Familienbeziehungen belasten. Die in der Regel noch gesunde Frau wird in der Beratung oft zum ersten Mal damit konfrontiert, dass die Erkrankung potenziell alle in der Familie und auch sie im Laufe ihres Lebens betreffen kann. Diese emotionale Belastung sollte in besonderer Weise berücksichtigt werden. Dabei ist innerhalb der Familie die Autonomie aller mit einem Recht auf Wissen, aber auch Nichtwissen sicherzustellen.


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