CYB5D2 displays tumor suppression activities towards cervical cancer

Xie, Yanyun; Shen, Yen Ting; Kapoor, Anil; Ojo, Diane; Wei, Fengxiang; Melo, Jason De; Lin, Xiaozeng; Wong, Nicholas; Yan, Judy; Tao, Ling; Major, Pierre; Tang, Damu

doi:10.1016/j.bbadis.2015.12.013

Cited by 11 publications

(17 citation statements)

References 42 publications

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“…In addition, NR2F1, an orphan nuclear receptor, has been confirmed to induce quiescence of disseminated tumor cells 22 . It has also been reported that CYB5D2 possesses tumor-suppressing activity and significantly inhibits cell invasion in vitro and cell-produced lung metastasis in vivo 23 . Additionally, the homozygous loss-of- function germline mutation in the NTHL1 gene is related to a new subtype of base-excision repair-associated adenomatous polyposis and colorectal cancer 24 .…”

Section: Resultsmentioning

confidence: 94%

Integrative analysis of copy number and transcriptional expression profiles in esophageal cancer to identify a novel driver gene for therapy

Dong

Mao

et al. 2017

Sci Rep

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An increasing amount of evidence has highlighted the critical roles that copy number variants play in cancer progression. Here, we systematically analyzed the copy number alterations and differentially transcribed genes. Integrative analysis of the association between copy number variants and differential gene expression suggested that copy number variants will lead to aberrant expression of the corresponding genes. We performed a KEGG pathway and GO analysis, which revealed that cell cycle may have an effective role in the progression of esophageal cancer. FAM60A was then screened out as a potential prognostic factor through survival analysis and correlation analysis with clinical-pathological parameters. We subsequently showed that silencing of FAM60A could inhibit esophageal carcinoma tumor cell growth, migration and invasion in vitro. Through the bioinformatic analysis, we predict that FAM60A may act as a transcriptional factor to regulate genes that are correlated with each cell cycle. In summary, we comprehensively analyzed copy number segments and transcriptional expression profiles, which provided a novel approach to identify clinical biomarkers and therapeutic targets of esophageal carcinoma.

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Section: Resultsmentioning

confidence: 94%

Integrative analysis of copy number and transcriptional expression profiles in esophageal cancer to identify a novel driver gene for therapy

Dong

Mao

et al. 2017

Sci Rep

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“…Built on the seminal detection of HPV16 DNA in 61.1% (11/18) of cervical cancers in 1983 [61], it became clear that infection by HPV is the primary etiology of cervix carcinoma, particularly with the high-risk HPV types 16 and 18 [62]. Besides HPV infection, alterations in cellular oncogenic events are also required for cervical cancer [63]. The integration of both HPV16 and HPV18 at the gene desert suggests that HPV coordinately affects oncogene alterations for cervical cancer formation [13,[64][65][66][67].…”

Section: Association Of the 8q2421 Gene Desert With Oncogenesismentioning

confidence: 99%

The Oncogenic Potential of the Centromeric Border Protein FAM84B of the 8q24.21 Gene Desert

Lin

Kapoor

et al. 2020

Genes

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FAM84B is a risk gene in breast and prostate cancers. Its upregulation is associated with poor prognosis of prostate cancer, breast cancer, and esophageal squamous cell carcinoma. FAM84B facilitates cancer cell proliferation and invasion in vitro, and xenograft growth in vivo. The FAM84B and Myc genes border a 1.2 Mb gene desert at 8q24.21. Co-amplification of both occurs in 20 cancer types. Mice deficient of a 430 Kb fragment within the 1.2 Mb gene desert have downregulated FAM84B and Myc expressions concurrent with reduced breast cancer growth. Intriguingly, Myc works in partnership with other oncogenes, including Ras. FAM84B shares similarities with the H-Ras-like suppressor (HRASLS) family over their typical LRAT (lecithin:retinal acyltransferase) domain. This domain contains a catalytic triad, H23, H35, and C113, which constitutes the phospholipase A 1/2 and O-acyltransferase activities of HRASLS1-5. These enzymatic activities underlie their suppression of Ras. FAM84B conserves H23 and H35 but not C113 with both histidine residues residing within a highly conserved motif that FAM84B shares with HRASLS1-5. Deletion of this motif abolishes FAM84B oncogenic activities. These properties suggest a collaboration of FAM84B with Myc, consistent with the role of the gene desert in strengthening Myc functions. Here, we will discuss recent research on FAM84B-derived oncogenic potential.Genes 2020, 11, 312 2 of 15 non-coding RNA (lnRNA), and on its upstream or centromeric side sits a 1.2 Mb gene desert with the centromeric side bordered by the FAM84B or LRATD2 gene ( Figure 1). The unique feature of this gene desert is the existence of multiple (lnRNAs) (PCAT1, PCAT2, POU5F1B, CCAT1, CCAT2, CASC8, CASC11, CASC19, and CASC21) with FAM84B and Myc being the only protein coding genes (Figure 1) [12][13][14]. In view of Myc being the most-well-studied oncogene and the 8q24 gene desert as a region that is frequently amplified in cancer, FAM84B stands as a promising target for oncogenic activities; nonetheless, its impact on tumorigenesis remained unknown until recently. As the oncogenic potential of the non-coding RNAs of PVT1 and those within the gene desert (Figure 1) has been recently reviewed [13][14][15][16][17], we will focus on the emerging role of FAM84B in tumorigenesis in this review. We will briefly discuss the 8q24 gene desert with respect to oncogenesis to set the stage for the following systemic examination of the evidence pertinent to FAM84B-derived tumorigenesis. The main materials used in this review were chosen based on the PRISMA (preferred reporting items for systematic reviews and meta-analyses) Guidelines [18,19]. A literature search of the PubMed database for (1) "8q24 gene desert", revealed 28 papers with 6 irrelevant to tumorigenesis (Figure 2A) and (2) "FAM84B", identified 21 articles, including non-English papers (n = 1) and articles not directly related to FAM84B and cancer (n = 2) ( Figure 2B). After excluding these items, 22 articles on 8q24 gene desert and 18 papers related to the FAM84B topic h...

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“…Despite considerable advances in understanding the molecular basis of abdominal and pelvic neoplasms, abdominal and pelvic cancers, such as colorectal cancer, prostate cancer and cervical cancer, remain the most common form of cancer leading tumor-related mortality globally [1]; [2]; [3]. Radiotherapy is a cornerstone of modern management of malignancies and, > 50% of patients with cancer receive this treatment at some point in the course of their disease [4].…”

Section: Introductionmentioning

confidence: 99%

Total abdominal irradiation exposure impairs cognitive function involving miR-34a-5p/BDNF axis

Cui¹,

Xiao²,

Li³

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Radiotherapy is often employed to treat abdominal and pelvic malignancies, but is frequently accompanied by diverse acute and chronic local injuries. It was previously unknown whether abdominal and pelvic radiotherapy impairs distant cognitive dysfunction. In the present study, we demonstrated that total abdominal irradiation (TAI) exposure caused cognitive deficits in mouse models. Mechanically, microarray assay analysis revealed that TAI elevated the expression level of miR-34a-5p in small intestine tissues and peripheral blood (PD), which targeted the 3′UTR of Brain-derived neurotrophic factor (Bdnf) mRNA in hippocampus to mediate cognitive dysfunction. Tail intravenous injection of miR-34a-5p antagomir immediately after TAI exposure rescued TAI-mediated cognitive impairment via blocking the up-regulation of miR-34a-5p in PD, resulting in restoring the Bdnf expression in the hippocampus. More importantly, high throughput sequencing validated that the gut bacterial composition of mice was shifted after TAI exposure, which was retained by miR-34a-5p antagomir injection. Thus, 27(7):916-932our findings provide new insights into pathogenic mechanism underlying abdominal and pelvic radiotherapy-mediated distant cognitive impairment.

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CYB5D2 displays tumor suppression activities towards cervical cancer

Cited by 11 publications

References 42 publications

Integrative analysis of copy number and transcriptional expression profiles in esophageal cancer to identify a novel driver gene for therapy

Integrative analysis of copy number and transcriptional expression profiles in esophageal cancer to identify a novel driver gene for therapy

The Oncogenic Potential of the Centromeric Border Protein FAM84B of the 8q24.21 Gene Desert

Total abdominal irradiation exposure impairs cognitive function involving miR-34a-5p/BDNF axis

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