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HOX Genes in Development and Disease
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HOX Genes in Development and Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 12791

Special Issue Editor

Dr. Alfredo Procino

E-Mail Website
Guest Editor
Department of Clinical Medicine and Surgery - Medical School "Federico II" of Naples, 80131 Naples Italy
Interests: HOX genes; cancer biology; molecular biology

Special Issue Information

Dear Colleagues,

Breast cancer represents one of the most common cancers in women, second only to skin cancer. The mortality risk from breast cancer is 1 in 37 women (2.7%), which makes breast cancer represent the second cause of cancer death in women. Recently, new research works based on previously published work in systemic chemotherapy and endocrine therapy have improved the incidence rates. The quinonic nucleus is common to many natural and synthetic products associated with anticancer and antibacterial activities; these compounds are typically DNA-intercalating agents. The HOX genes control embryonic development and the specific determination of positional identity in the anteroposterior axis of the human body. The HOX genes are 39 transcription factors related to morphological and physiological disease. It has been demonstrated that any deregulation in the network is able to induce neoplastic transformation. Particularly, the HOXC locus in collaboration with the lncRNA HOTAIR plays a key role in breast cancer. In this Special Issue we are interested in receiving new research data in order to evaluate the chemical and metabolic stability of new anticancer molecules.

Dr. Alfredo Procino
Guest Editor

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Keywords

  • HOX genes
  • anti-cancer drugs
  • cell memory program

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Published Papers (4 papers)

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Research

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16 pages, 3228 KiB  
Article
HOXA9 Overexpression Contributes to Stem Cell Overpopulation That Drives Development and Growth of Colorectal Cancer
by Brian Osmond, Caroline O. B. Facey, Chi Zhang and Bruce M. Boman
Int. J. Mol. Sci. 2022, 23(12), 6799; https://doi.org/10.3390/ijms23126799 - 18 Jun 2022
Cited by 10 | Viewed by 2229
Abstract
HOX proteins are transcription factors that regulate stem cell (SC) function, but their role in the SC origin of cancer is under-studied. Aberrant expression of HOX genes occurs in many cancer types. Our goal is to ascertain how retinoic acid (RA) signaling and [...] Read more.
HOX proteins are transcription factors that regulate stem cell (SC) function, but their role in the SC origin of cancer is under-studied. Aberrant expression of HOX genes occurs in many cancer types. Our goal is to ascertain how retinoic acid (RA) signaling and the regulation of HOXA9 expression might play a role in the SC origin of human colorectal cancer (CRC). Previously, we reported that aldehyde dehydrogenase (ALDH) and other RA pathway components are co-expressed in colonic cancer SCs (CSCs) and that overpopulation of ALDH-positive CSCs occurs during colon tumorigenesis. Our hypothesis is RA signaling regulates HOXA9 expression, and dysregulated RA signaling results in HOXA9 overexpression, which contributes to CSC overpopulation in CRC. Immunostaining showed that HOXA9 was selectively expressed in ALDH-positive SCs, and HOXA9 expression was increased in CRCs compared to normal epithelium. Modulating RA signaling in CRC cells (HT29 and SW480) with ATRA and DEAB decreased cell proliferation and reduced HOXA9 expression. Bioinformatics analyses identified a network of proteins that functionally interact with HOXA9, and the genes that encode these proteins, as well as HOXA9, contain RA receptor binding sites. These findings indicate that the expression of HOXA9 and its functional network is regulated by RA signaling in normal colonic SCs, and, when dysregulated, HOXA9 may contribute to CSC overpopulation that drives CRC development and growth. Our study provides a regulatory mechanism that might be useful in developing treatments against CSC overpopulation in CRC. Full article
(This article belongs to the Special Issue HOX Genes in Development and Disease)
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14 pages, 1788 KiB  
Article
HOXC6-Mediated miR-188-5p Expression Induces Cell Migration through the Inhibition of the Tumor Suppressor FOXN2
by Seho Jeong, Soo-A Kim and Sang-Gun Ahn
Int. J. Mol. Sci. 2022, 23(1), 9; https://doi.org/10.3390/ijms23010009 - 21 Dec 2021
Cited by 15 | Viewed by 2137
Abstract
Homeobox C6 (HOXC6) is a transcription factor that plays a role in the malignant progression of various cancers. However, the roles of HOXC6 and its regulatory mechanism remain unclear. In this study, we used microRNA (miRNA) regulatory networks to identify key regulatory interactions [...] Read more.
Homeobox C6 (HOXC6) is a transcription factor that plays a role in the malignant progression of various cancers. However, the roles of HOXC6 and its regulatory mechanism remain unclear. In this study, we used microRNA (miRNA) regulatory networks to identify key regulatory interactions responsible for HOXC6-mediated cancer progression. In microarray profiling of miRNAs, the levels of miRNAs such as hsa-miR-188-5p, hsa-miR-8063, and hsa-miR-8064 were significantly increased in HOXC6-overexpressing cells. Higher positive expression rates of HOXC6 and miR-188-5p were observed in malignant cancer. We also found that HOXC6 significantly upregulated miR-188-5p expression. The underlying function of HOXC6-mediated miR-188-5p expression was predicted through TargetScan and the MiRNA Database. Overexpression of mir-188-5p inhibited the expression of forkhead box N2 (FOXN2), a tumor suppressor gene. Furthermore, in the luciferase assay, miR-188-5p bound to the 3′-UTR of FOXN2 and was mainly responsible for the dysregulation of FOXN2 expression. Silencing FOXN2 induced cell migration, and the effect of FOXN2 silencing was enhanced when the HOXC6/miR-188-5p axis was induced. These results suggest that HOXC6/miR-188-5p may induce malignant progression in cancer by inhibiting the activation of the FOXN2 signaling pathway. Full article
(This article belongs to the Special Issue HOX Genes in Development and Disease)
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19 pages, 5224 KiB  
Article
HOXB8 Counteracts MAPK/ERK Oncogenic Signaling in a Chicken Embryo Model of Neoplasia
by Axelle Wilmerding, Lauranne Bouteille, Lucrezia Rinaldi, Nathalie Caruso, Yacine Graba and Marie-Claire Delfini
Int. J. Mol. Sci. 2021, 22(16), 8911; https://doi.org/10.3390/ijms22168911 - 18 Aug 2021
Cited by 4 | Viewed by 2744
Abstract
HOX transcription factors are members of an evolutionarily conserved family of proteins required for the establishment of the anteroposterior body axis during bilaterian development. Although they are often deregulated in cancers, the molecular mechanisms by which they act as oncogenes or tumor suppressor [...] Read more.
HOX transcription factors are members of an evolutionarily conserved family of proteins required for the establishment of the anteroposterior body axis during bilaterian development. Although they are often deregulated in cancers, the molecular mechanisms by which they act as oncogenes or tumor suppressor genes are only partially understood. Since the MAPK/ERK signaling pathway is deregulated in most cancers, we aimed at apprehending if and how the Hox proteins interact with ERK oncogenicity. Using an in vivo neoplasia model in the chicken embryo consisting in the overactivation of the ERK1/2 kinases in the trunk neural tube, we analyzed the consequences of the HOXB8 gain of function at the morphological and transcriptional levels. We found that HOXB8 acts as a tumor suppressor, counteracting ERK-induced neoplasia. The HOXB8 tumor suppressor function relies on a large reversion of the oncogenic transcriptome induced by ERK. In addition to showing that the HOXB8 protein controls the transcriptional responsiveness to ERK oncogenic signaling, our study identified new downstream targets of ERK oncogenic activation in an in vivo context that could provide clues for therapeutic strategies. Full article
(This article belongs to the Special Issue HOX Genes in Development and Disease)
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Review

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22 pages, 1081 KiB  
Review
The Role of lncRNAs in Rare Tumors with a Focus on HOX Transcript Antisense RNA (HOTAIR)
by Giuseppina Liguori, Margherita Cerrone, Annarosaria De Chiara, Salvatore Tafuto, Maura Tracey de Bellis, Gerardo Botti, Maurizio Di Bonito and Monica Cantile
Int. J. Mol. Sci. 2021, 22(18), 10160; https://doi.org/10.3390/ijms221810160 - 21 Sep 2021
Cited by 6 | Viewed by 4757
Abstract
Rare cancers are identified as those with an annual incidence of fewer than 6 per 100,000 persons and includes both epithelial and stromal tumors from different anatomical areas. The advancement of analytical methods has produced an accurate molecular characterization of most human cancers, [...] Read more.
Rare cancers are identified as those with an annual incidence of fewer than 6 per 100,000 persons and includes both epithelial and stromal tumors from different anatomical areas. The advancement of analytical methods has produced an accurate molecular characterization of most human cancers, suggesting a “molecular classification” that has allowed the establishment of increasingly personalized therapeutic strategies. However, the limited availability of rare cancer samples has resulted in very few therapeutic options for these tumors, often leading to poor prognosis. Long non coding RNAs (lncRNAs) are a class of non-coding RNAs mostly involved in tumor progression and drug response. In particular, the lncRNA HOX transcript antisense RNA (HOTAIR) represents an emergent diagnostic, prognostic and predictive biomarker in many human cancers. The aim of this review is to highlight the role of HOTAIR in rare cancers, proposing it as a new biomarker usable in the management of these tumors. Full article
(This article belongs to the Special Issue HOX Genes in Development and Disease)
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