Highly heterogeneous-related genes of triple-negative breast cancer: potential diagnostic and prognostic biomarkers

Liu, Yiduo; Teng, Linxin; Fu, Shiyi; Wang, Guiyang; Li, Zhengjun; Ding, Chao; Wang, Haodi; Bi, Lei

doi:10.1186/s12885-021-08318-1

Cited by 18 publications

(12 citation statements)

References 79 publications

(69 reference statements)

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“…Consistently, a decrease in FAM83B expression was also found in the metastatic tissue with respect to the corresponding primary tumor, which was more evident and significant in distant metastases from FTCs, than in locoregional recurrences from PTCs. Moreover, patients with low FAM83B levels tended to have a higher frequency of distant metastatization and a shorter DFS rate than those with high levels, further highlighting the correlation between dedifferentiation and low FAM83B mRNA levels, and consistent with data found in ovarian cancer 8 , in lung squamous cell carcinoma—SCC 9 , and triple-negative breast cancer 20 .…”

Section: Discussionsupporting

confidence: 83%

“…FAM83A , FAM83D , FAM83G , and FAM83H ) have been reported to be involved in the regulation of cell migration in different tumors (osteosarcoma, endometrial, colon, cervical and gastric cancer) 12 , 15 – 19 . On the other hand, it has been very recently reported that ovarian cancer patients with low FAM83B levels have shorter survival time and show cisplatin resistance 8 , while high expression of FAM83B correlates with prolonged progression-free interval in triple negative breast cancer 20 .…”

Section: Introductionmentioning

confidence: 99%

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FAM83B is involved in thyroid cancer cell differentiation and migration

Cirello

Grassi

Pogliaghi

et al. 2022

Sci Rep

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FAM83B has been recently identified as an oncogene, but its role in thyroid cancers (TC) is still unclear. We examined the expression of FAM83B and its possible involvement in cell migration and differentiation, in neoplastic/normal thyroid tissues and in TC human cell lines. FAM83B expression in TC varies according to the tumor histotype, being significantly downregulated in more aggressive and metastatic tissues. FAM83B levels in cell lines recapitulate patients’ samples variations, and its total and cytoplasmic levels decrease upon the induction of migration, together with an increase in its nuclear localization. Similar variations were detected in the primary tumor and in the metastatic tissues from a follicular TC. FAM83B knock down experiments confirmed its role in thyroid differentiation and cell migration, as demonstrated by the reduction of markers of thyroid differentiation and the increase of the mesenchymal marker vimentin. Moreover, the silencing of FAM83B significantly increased cells migration abilities, while not affecting the oncogenic RAS/MAPK/PI3K pathways. Our data indicate for the first time a role for FAM83B in TC cell differentiation and migration. Its expression is reduced in dedifferentiated tumors and its nuclear re-localization could favour distant migration, suggesting that FAM83B should be considered a possible diagnostic and prognostic biomarker.

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Section: Discussionsupporting

confidence: 83%

Section: Introductionmentioning

confidence: 99%

FAM83B is involved in thyroid cancer cell differentiation and migration

Cirello

Grassi

Pogliaghi

et al. 2022

Sci Rep

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“…Recently, several prognostic factors have been identified in previous research with the aim of helping decision-making in pursuit of tailored individual care for TNBC patients. Yiduo Liu et al screened four heterogeneous-related genes (FAM83B, KITLG, RBM24, and S100B) from 105 genes to construct a prognostic signature in the disease-free interval (DFI) of TNBC (16). Chao Li et al identified a prognosis-related signature associated with energy metabolism including eight energy metabolism-associated genes (IL1RL2, FBLN7, CA3, PDE1B, SLURP1, CILP, AQP7, and TPSB) in triple-negative breast cancer (17).…”

Section: Discussionmentioning

confidence: 99%

Construction and Validation of a Prognostic Risk Model for Triple-Negative Breast Cancer Based on Autophagy-Related Genes

2022

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BackgroundAutophagy plays an important role in triple-negative breast cancer (TNBC). However, the prognostic value of autophagy-related genes (ARGs) in TNBC remains unknown. In this study, we established a survival model to evaluate the prognosis of TNBC patients using ARGs signature.MethodsA total of 222 autophagy-related genes were downloaded from The Human Autophagy Database. The RNA-sequencing data and corresponding clinical data of TNBC were obtained from The Cancer Genome Atlas (TCGA) database. Differentially expressed autophagy-related genes (DE-ARGs) between normal samples and TNBC samples were determined by the DESeq2 package. Then, univariate Cox, least absolute shrinkage and selection operator (LASSO), and multivariate Cox regression analyses were performed. According to the LASSO regression results based on univariate Cox, we identified a prognostic signature for overall survival (OS), which was further validated by using the Gene Expression Omnibus (GEO) cohort. We also found an independent prognostic marker that can predict the clinicopathological features of TNBC. Furthermore, a nomogram was drawn to predict the survival probability of TNBC patients, which could help in clinical decision for TNBC treatment. Finally, we validated the requirement of an ARG in our model for TNBC cell survival and metastasis.ResultsThere are 43 DE-ARGs identified between normal and tumor samples. A risk model for OS using CDKN1A, CTSD, CTSL, EIF4EBP1, TMEM74, and VAMP3 was established based on univariate Cox regression and LASSO regression analysis. Overall survival of TNBC patients was significantly shorter in the high-risk group than in the low-risk group for both the training and validation cohorts. Using the Kaplan–Meier curves and receiver operating characteristic (ROC) curves, we demonstrated the accuracy of the prognostic model. Multivariate Cox regression analysis was used to verify risk score as an independent predictor. Subsequently, a nomogram was proposed to predict 1-, 3-, and 5-year survival for TNBC patients. The calibration curves showed great accuracy of the model for survival prediction. Finally, we found that depletion of EIF4EBP1, one of the ARGs in our model, significantly reduced cell proliferation and metastasis of TNBC cells.ConclusionBased on six ARGs (CDKN1A, CTSD, CTSL, EIF4EBP1, TMEM74, and VAMP3), we developed a risk prediction model that can help clinical doctors effectively predict the survival status of TNBC patients. Our data suggested that EIF4EBP1 might promote the proliferation and migration in TNBC cell lines. These findings provided a novel insight into the vital role of the autophagy-related genes in TNBC and may provide new therapeutic targets for TNBC.

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“…For example, survival analyses suggest that RBM24 may be a potential prognostic biomarker for head and neck squamous cell carcinoma (HNSCC) and skin cutaneous melanoma (SKCM) patients [ 58 , 59 ]. In triple negative breast cancer (TNBC) patients, RBM24 is upregulated during the disease-free interval (DFI) and is correlated with poor prognosis [ 34 ]. In medulloblastoma (MB), RBM24 represents one of the few reliable biomarkers that can be used for diagnosis and prognosis of group 4 tumors [ 60 ].…”

Section: Rbm24 In Cancer Developmentmentioning

confidence: 99%

“…Functional and correlative analyses suggest that it displays either anti-oncogenic or oncogenic potential. Several studies suggest that it suppresses tumor progression [ 28 , 29 , 30 , 31 , 32 ], while others indicate that its upregulation promotes tumor growth [ 33 , 34 , 35 , 36 , 37 ]. These raise the possibility that RBM24 may act either as a tumor suppressor or as an oncogene, functioning in a context- or background-dependent manner.…”

Section: Introductionmentioning

confidence: 99%

RBM24 in the Post-Transcriptional Regulation of Cancer Progression: Anti-Tumor or Pro-Tumor Activity?

Shi

2022

Cancers

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RNA-binding proteins are critical post-transcriptional regulators of gene expression. They are implicated in a wide range of physiological and pathological processes by modulating nearly every aspect of RNA metabolisms. Alterations in their expression and function disrupt tissue homeostasis and lead to the occurrence of various cancers. RBM24 is a highly conserved protein that binds to a large spectrum of target mRNAs and regulates many post-transcriptional events ranging from pre-mRNA splicing to mRNA stability, polyadenylation and translation. Studies using different animal models indicate that it plays an essential role in promoting cellular differentiation during organogenesis and tissue regeneration. Evidence is also accumulating that its dysregulation frequently occurs across human cancers. In several tissues, RBM24 clearly functions as a tumor suppressor, which is consistent with its inhibitory potential on cell proliferation. However, upregulation of RBM24 in other cancers appears to promote tumor growth. There is a possibility that RBM24 displays both anti-tumor and pro-tumor activities, which may be regulated in part through differential interactions with its protein partners and by its post-translational modifications. This makes it a potential biomarker for diagnosis and prognosis, as well as a therapeutic target for cancer treatment. The challenge remains to determine the post-transcriptional mechanisms by which RBM24 modulates gene expression and tumor progression in a context- or background-dependent manner. This review discusses recent findings on the potential function of RBM24 in tumorigenesis and provides future directions for better understanding its regulatory role in cancer cells.

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Highly heterogeneous-related genes of triple-negative breast cancer: potential diagnostic and prognostic biomarkers

Cited by 18 publications

References 79 publications

FAM83B is involved in thyroid cancer cell differentiation and migration

FAM83B is involved in thyroid cancer cell differentiation and migration

Construction and Validation of a Prognostic Risk Model for Triple-Negative Breast Cancer Based on Autophagy-Related Genes

RBM24 in the Post-Transcriptional Regulation of Cancer Progression: Anti-Tumor or Pro-Tumor Activity?

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