Identification and gastrointestinal expression of Xenopus laevis FoxF2

Mclin, Valérie Anne; Shah, Rina; Desai, Neekita P.; Jamrich, Milan

doi:10.1387/ijdb.092916vm

Cited by 4 publications

(3 citation statements)

References 24 publications

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“…The FoxF2 expression has been found in the mesenchyme of the oral cavity, limb buds, genitalia, central nervous system, eyes, lung, prostate, ear and placenta as well as the lamina propria and smooth muscle of the GI tract (30, 31). FoxF2 was shown to be a target of miR-200 family in lung cancer and its expression in lung tumor cells increased invasion and metastasis, indicating an oncogenic role of FoxF2 in lung cancer (32).…”

Section: Introductionmentioning

confidence: 99%

FoxF1 and FoxF2 transcription factors synergistically promote rhabdomyosarcoma carcinogenesis by repressing transcription of p21Cip1 CDK inhibitor

et al. 2016

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The role of Forkhead Box F1 (FoxF1) transcription factor in carcinogenesis is not well characterized. Depending on tissue and histological type of cancer, FoxF1 was shown to be either oncogene or tumor suppressor. Alveolar rhabdomyosarcoma (RMS) is the most aggressive pediatric soft tissue sarcoma. While FoxF1 is highly expressed in alveolar RMS, the functional role of FoxF1 in RMS is unknown. The present study demonstrates that expression of FoxF1 and its closely related transcription factor FoxF2 are essential for rhabdomyosarcoma tumor growth. Depletion of FoxF1 or FoxF2 in rhabdomyosarcoma cells decreased tumor growth in orthotopic mouse models of RMS. The decreased tumorigenesis was associated with the reduced tumor cell proliferation. Cell cycle regulatory proteins Cdk2, Cdk4/6, Cyclin D1 and Cyclin E2 were decreased in FoxF1- and FoxF2-deficient RMS tumors. Depletion of either FoxF1 or FoxF2 delayed G1-S cell cycle progression, decreased levels of phosphorylated Rb and increased protein levels of the CDK inhibitors, p21Cip1 and p27Kip1. Depletion of both FoxF1 and FoxF2 in tumor cells completely abrogated RMS tumor growth in mice. Overexpression of either FoxF1 or FoxF2 in tumor cells was sufficient to increase carcinogenesis in orthotopic RMS mouse model. FoxF1 and FoxF2 directly bound to and repressed transcriptional activity of p21Cip1 promoter through −556/−545 bp region, but did not affect p27Kip1 transcription. Knockdown of p21Cip1 restored cell cycle progression in the FoxF1- or FoxF2-deficient tumor cells. Altogether, FoxF1 and FoxF2 promoted RMS tumorigenesis by inducing tumor cell proliferation via transcriptional repression of p21Cip1 gene promoter. Due to robust oncogenic activity in RMS tumors, FoxF1 and FoxF2 may represent promising targets for anti-tumor therapy.

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Section: Introductionmentioning

confidence: 99%

FoxF1 and FoxF2 transcription factors synergistically promote rhabdomyosarcoma carcinogenesis by repressing transcription of p21Cip1 CDK inhibitor

et al. 2016

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“…Several Fox proteins, including Foxo4, Foxq1, and Foxf1, have been shown to be critical for smooth muscle cell development via regulation of the myocardin/serum response factor (SRF) axis (18 -20). Using in situ hybridization, embryonic Foxf2 expression has been found in the mesenchyme of the oral cavity, limb buds, genitalia, CNS, eyes, lung, prostate, ear, and placenta as well as the lamina propria region and smooth muscle of the developing GI tract (21,22). During embryonic development, Hedgehog signaling from the epithelium induces Foxf2 expression (17); however, postnatal Foxf2 expression and signaling remain poorly characterized.…”

mentioning

confidence: 99%

Forkhead Box F2 Regulation of Platelet-derived Growth Factor and Myocardin/Serum Response Factor Signaling Is Essential for Intestinal Development

Bolte

Ren

Tomley

et al. 2015

Journal of Biological Chemistry

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Background: Transcriptional regulation of smooth muscle cells is an understudied component of intestinal development and physiology. Results: Foxf2 deletion from smooth muscle causes intestinal malformations and colon remodeling. Conclusion: Foxf2 regulation of PDGF and myocardin/SRF signaling is essential for intestinal development and homeostasis. Significance: Better understanding of transcriptional mechanisms regulating postnatal intestine development and homeostasis may provide therapeutic approaches for congenital and acquired gastrointestinal diseases.

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“…1) [66][67][68][69]. Foxf2 -/-and Foxf2 ?/-mouse embryos show multi-visceral abnormalities, including colorectal muscle hypoplasia.…”

Section: Signaling Pathways and Transcription Factors Involved In Gi mentioning

confidence: 99%

Mesenchymal–epithelial interactions during digestive tract development and epithelial stem cell regeneration

Guen

Marchal

Faure

et al. 2015

Cell. Mol. Life Sci.

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The gastrointestinal tract develops from a simple and uniform tube into a complex organ with specific differentiation patterns along the anterior-posterior and dorso-ventral axes of asymmetry. It is derived from all three germ layers and their cross-talk is important for the regulated development of fetal and adult gastrointestinal structures and organs. Signals from the adjacent mesoderm are essential for the morphogenesis of the overlying epithelium. These mesenchymal-epithelial interactions govern the development and regionalization of the different gastrointestinal epithelia and involve most of the key morphogens and signaling pathways, such as the Hedgehog, BMPs, Notch, WNT, HOX, SOX and FOXF cascades. Moreover, the mechanisms underlying mesenchyme differentiation into smooth muscle cells influence the regionalization of the gastrointestinal epithelium through interactions with the enteric nervous system. In the neonatal and adult gastrointestinal tract, mesenchymal-epithelial interactions are essential for the maintenance of the epithelial regionalization and digestive epithelial homeostasis. Disruption of these interactions is also associated with bowel dysfunction potentially leading to epithelial tumor development. In this review, we will discuss various aspects of the mesenchymal-epithelial interactions observed during digestive epithelium development and differentiation and also during epithelial stem cell regeneration.

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Identification and gastrointestinal expression of Xenopus laevis FoxF2

Cited by 4 publications

References 24 publications

FoxF1 and FoxF2 transcription factors synergistically promote rhabdomyosarcoma carcinogenesis by repressing transcription of p21Cip1 CDK inhibitor

FoxF1 and FoxF2 transcription factors synergistically promote rhabdomyosarcoma carcinogenesis by repressing transcription of p21Cip1 CDK inhibitor

Forkhead Box F2 Regulation of Platelet-derived Growth Factor and Myocardin/Serum Response Factor Signaling Is Essential for Intestinal Development

Mesenchymal–epithelial interactions during digestive tract development and epithelial stem cell regeneration

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