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Heldin, P., Kolliopoulos, C., Lin, C.-Y. & Heldin, C.-H. (2020). Involvement of hyaluronan and CD44 in cancer and viral infections. Cellular Signalling, 65, Article ID 109427.
Open this publication in new window or tab >>Involvement of hyaluronan and CD44 in cancer and viral infections
2020 (English)In: Cellular Signalling, ISSN 0898-6568, E-ISSN 1873-3913, Vol. 65, article id 109427Article in journal (Refereed) Published
Abstract [en]

Hyaluronan and its major receptor CD44 are ubiquitously distributed. They have important structural as well as signaling roles, regulating tissue homeostasis, and their expression levels are tightly regulated. In addition to signaling initiated by the interaction of the intracellular domain of CD44 with cytoplasmic signaling molecules, CD44 has important roles as a co-receptor for different types of receptors of growth factors and cytokines. Dysregulation of hyaluronan-CD44 interactions is seen in diseases, such as inflammation and cancer. In the present communication, we discuss the mechanism of hyaluronan-induced signaling via CD44, as well as the involvement of hyaluronan-engaged CD44 in malignancies and in viral infections.

Place, publisher, year, edition, pages
ELSEVIER SCIENCE INC, 2020
Keywords
CD44, Hyaluronan, Receptor tyrosine kinase, Viral infection, Proteolytic cleavage, EMT
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-400721 (URN)10.1016/j.cellsig.2019.109427 (DOI)000501657400009 ()31654718 (PubMedID)
Funder
Swedish Cancer Society, 2015-0778Swedish Research Council, 2015-02757
Available from: 2020-01-28 Created: 2020-01-28 Last updated: 2020-01-28Bibliographically approved
Tsioumpekou, M., Cunha, S. I., Ma, H., Åhgren, A., Cedervall, J., Olsson, A.-K., . . . Lennartsson, J. (2020). Specific targeting of PDGFR beta in the stroma inhibits growth and angiogenesis in tumors with high PDGF-BB expression. Theranostics, 10(3), 1122-1135
Open this publication in new window or tab >>Specific targeting of PDGFR beta in the stroma inhibits growth and angiogenesis in tumors with high PDGF-BB expression
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2020 (English)In: Theranostics, ISSN 1838-7640, E-ISSN 1838-7640, Vol. 10, no 3, p. 1122-1135Article in journal (Refereed) Published
Abstract [en]

PDGF-BB/PDGFR beta signaling plays an important role during vascularization by mediating pericyte recruitment to the vasculature, promoting the integrity and function of vessels. Until now it has not been possible to assess the specific role of PDGFR beta signaling in tumor progression and angiogenesis due to lack of appropriate animal models and molecular tools. Methods: In the present study, we used a transgenic knock-in mouse strain carrying a silent mutation in the PDGFR beta ATP binding site that allows specific targeting of PDGFR beta using the compound 1-NaPP1. To evaluate the impact of selective PDGFR beta inhibition of stromal cells on tumor growth we investigated four tumor cell lines with no or low PDGFR beta expression, i.e. Lewis lung carcinoma (LLC), EO771 breast carcinoma, B16 melanoma and a version of B16 that had been engineered to overexpress PDGF-BB (B16/PDGF-BB). Results: We found that specific impairment of PDGFR beta kinase activity by 1-NaPP1 treatment efficiently suppressed growth in tumors with high expression of PDGF-BB, i.e. LLC and B16/PDGF-BB, while the clinically used PDGFR beta kinase inhibitor imatinib did not suppress tumor growth. Notably, tumors with low levels of PDGF-BB, i.e. EO771 and B16, neither responded to 1-NaPP1 nor to imatinib treatment. Inhibition of PDGFR beta by either drug impaired tumor vascularization and also affected pericyte coverage; however, specific targeting of PDGFR beta by 1-NaPP1 resulted in a more pronounced decrease in vessel function with increased vessel apoptosis in high PDGF-BB expressing tumors, compared to treatment with imatinib. In vitro analysis of PDGFR beta ASKA mouse embryo fibroblasts and the mesenchymal progenitor cell line 10T1/2 revealed that PDGF-BB induced NG2 expression, consistent with the in vivo data. Conclusion: Specific targeting of PDGFR beta signaling significantly inhibits tumor progression and angiogenesis depending on PDGF-BB expression. Our data suggest that targeting PDGFR beta in the tumor stroma could have therapeutic value in patients with high tumor PDGF-BB expression.

Place, publisher, year, edition, pages
IVYSPRING INT PUBL, 2020
Keywords
Low molecular weight inhibitor, PDGFR beta, pericytes, tumor growth, angiogenesis
National Category
Cell and Molecular Biology Cancer and Oncology
Identifiers
urn:nbn:se:uu:diva-402371 (URN)10.7150/thno.37851 (DOI)000503870400011 ()31938055 (PubMedID)
Funder
Swedish Cancer Society, 2018/425Swedish Cancer Society, 2015/445Lars Hierta Memorial FoundationStiftelsen Längmanska kulturfonden
Available from: 2020-02-03 Created: 2020-02-03 Last updated: 2020-02-03Bibliographically approved
Zarei, O., Sarri, N., Dastmalchi, S., Zokai, F., Papadopoulos, N., Lennartsson, J., . . . Hamzeh-Mivehroud, M. (2020). Structure-based discovery of novel small molecule inhibitors of platelet-derived growth factor-B. Bioorganic chemistry (Print), 94, Article ID 103374.
Open this publication in new window or tab >>Structure-based discovery of novel small molecule inhibitors of platelet-derived growth factor-B
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2020 (English)In: Bioorganic chemistry (Print), ISSN 0045-2068, Vol. 94, article id 103374Article in journal (Refereed) Published
Abstract [en]

Platelet-derived growth factor (PDGF) is a family of growth factors with mitogenic and chemotactic activity. However, uncontrolled and overactivated PDGF signaling has been implicated in a variety of diseases, such as cancers and atherosclerosis. In this context, inhibition of PDGF-PDGFR signaling is of paramount importance in progression of such diseases. The purpose of the current study was to identify novel PDGF-B inhibitors using virtual screening methods. To this end, a combination of molecular modeling techniques such as molecular docking and dynamics simulation, as well as drug likeness filtering criteria, was applied to select anti-PDGF peptidomimetic candidates based on crystallography solved structure of an anti-PDGF-B monoclonal antibody named, MOR8457. In vitro biological assays of the selected compounds revealed two of them being active at micromolar IC50, concentrations. The presented work can provide a framework for systematic peptidomimetic identification for anti-PDGF-B agents from large chemical libraries.

Keywords
Virtual screening, Platelet-derived growth factor-B, Molecular docking, Molecular dynamics simulation, Anti-PDGF-B agents, MOR8457 antibody
National Category
Medicinal Chemistry
Identifiers
urn:nbn:se:uu:diva-403397 (URN)10.1016/j.bioorg.2019.103374 (DOI)000505596300030 ()31699389 (PubMedID)
Funder
Swedish Cancer Society, 2016/445Swedish Cancer Society, 2018/425
Note

Omid Zarei and Niki Sarri contributed equally to this work

Available from: 2020-01-29 Created: 2020-01-29 Last updated: 2020-01-29Bibliographically approved
Yin, R., Eger, G., Sarri, N., Rorsman, C., Heldin, C.-H. & Lennartsson, J. (2019). Dual specificity phosphatase (DUSP)-4 is induced by platelet-derived growth factor -BB in an Erk1/2-, STAT3- and p53-dependent manner. Biochemical and Biophysical Research Communications - BBRC, 519(3), 469-474
Open this publication in new window or tab >>Dual specificity phosphatase (DUSP)-4 is induced by platelet-derived growth factor -BB in an Erk1/2-, STAT3- and p53-dependent manner
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2019 (English)In: Biochemical and Biophysical Research Communications - BBRC, ISSN 0006-291X, E-ISSN 1090-2104, Vol. 519, no 3, p. 469-474Article in journal (Refereed) Published
Abstract [en]

Dual specificity phosphatase (DUSP) 4 has been described as a negative regulator of MAP kinase signaling, in particular for the ERK1/2 and JNK pathways. We found that DUSP4 expression was upregulated in response to prolonged platelet-derived growth factor (PDGF)-BB stimulation. The PDGF-BB-induced DUSP4 expression was dependent on ERK1/2, STAT3 and p53. We found that inhibition of ERK1/2 effectively reduced DUSP4 mRNA levels, whereas STAT3 was necessary for maintaining p53 expression. p53 has binding sites in the DUSP4 promoter and was found to promote DUSP4 expression.

Keywords
DUSP4, Erk1/2, Multifactor regulation, PDGF, STAT3, p53
National Category
Cell Biology
Identifiers
urn:nbn:se:uu:diva-400210 (URN)10.1016/j.bbrc.2019.09.014 (DOI)000506407800004 ()31526568 (PubMedID)
Funder
Swedish Cancer Society, 2018/425Swedish Cancer Society, 2016/445
Note

De 2 första författarna delar förstaförfattarskapet

Available from: 2019-12-19 Created: 2019-12-19 Last updated: 2020-03-24Bibliographically approved
Kolliopoulos, C., Lin, C.-Y., Heldin, C.-H., Moustakas, A. & Heldin, P. (2019). Has2 natural antisense RNA and Hmga2 promote Has2 expression during TGFβ-induced EMT in breast cancer. Matrix Biology, 80, 29-45
Open this publication in new window or tab >>Has2 natural antisense RNA and Hmga2 promote Has2 expression during TGFβ-induced EMT in breast cancer
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2019 (English)In: Matrix Biology, ISSN 0945-053X, E-ISSN 1569-1802, Vol. 80, p. 29-45Article in journal (Refereed) Published
Abstract [en]

The glycosaminoglycan hyaluronan has a crucial role in tissue organization and cell signaling. Hyaluronan accumulates in conjunction with rapid tissue remodeling during embryogenesis, as well as in inflammatory conditions and cancer. We report a negative correlation between the expression of genes encoding hyaluronan synthase HAS2, its natural antisense transcript HAS2-AS, the chromatin modulating factor HMGA2 and transforming growth factor-β (TGFβ), and survival of patients with invasive breast carcinomas. In mouse mammary epithelial cells, TGFβ activates Smad and non-Smad signaling pathways, resulting in the transcriptional induction of Has2, Has2as (the mouse ortholog of HAS2-AS) and Hmga2, as well as epithelial-mesenchymal transition (EMT)-promoting transcription factors, such as Snail. Importantly, Has2as abrogation suppressed the TGFβ induction of EMT markers, including Snai1, Hmga2, Fn1, and suppressed the mesenchymal phenotype. TGFβ induction of Hmga2, Has2as and Has2, and synthesis of hyaluronan were accompanied with activation of Akt and Erk1/2 MAP-kinase signaling and were required for breast cancer cell motility. Importantly, the hyaluronan receptor Cd44, but not Hmmr, was required for TGFβ-mediated EMT phenotype. Interestingly, Has2as was found to contribute to the maintenance of stem cell factors and breast cancer stemness. Our findings show that Has2as has a key role in TGFβ- and HAS2-induced breast cancer EMT, migration and acquisition of stemness.

Keywords
Cancer, EMT, Hyaluronan, Stemness, lncRNA
National Category
Cell and Molecular Biology Cancer and Oncology
Identifiers
urn:nbn:se:uu:diva-372431 (URN)10.1016/j.matbio.2018.09.002 (DOI)000471739100003 ()30194979 (PubMedID)
Funder
Swedish Cancer Society, 15 0778Swedish Research Council, 15 02757
Available from: 2019-01-07 Created: 2019-01-07 Last updated: 2019-08-15Bibliographically approved
Lin, C.-Y., Kolliopoulos, C., Huang, C.-H., Tenhunen, J., Heldin, C.-H., Chen, Y.-H. & Heldin, P. (2019). High levels of serum hyaluronan is an early predictor of dengue warning signs and perturbs vascular integrity. EBioMedicine, 48, 425-441
Open this publication in new window or tab >>High levels of serum hyaluronan is an early predictor of dengue warning signs and perturbs vascular integrity
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2019 (English)In: EBioMedicine, E-ISSN 2352-3964, Vol. 48, p. 425-441Article in journal (Refereed) Published
Abstract [en]

Background: A main pathological feature of severe dengue virus infection is endothelial hyper-permeability. The dengue virus nonstructural protein 1 (NS1) has been implicated in the vascular leakage that characterizes severe dengue virus infection, however, the molecular mechanisms involved are not known.

Methods: A cohort of 250 dengue patients has been followed from the onset of symptoms to the recovery phase. Set urn hyaluronan levels and several other clinical parameters were recorded. The effect of NS1 treatment of cultured fibroblasts and endothelial cells on the expressions of hyaluronan synthetic and catabolic enzymes and the hyaluronan receptor CD44, were determined, as have the effects on the formation of hyaluronan-rich matrices and endothelial permeability.

Findings: Elevated serum hyaluronan levels (70 ng/ml) during early infection was found to be an independent predictor for occurrence of warning signs, and thus severe dengue fever. High circulating levels of the viral protein NS1, indicative of disease severity, correlated with high concentrations of serum hyaluronan. NS1 exposure decreased the expression of CD44 in differentiating endothelial cells impairing the integrity of vessel-like structures, and promoted the synthesis of hyaluronan in dermal fibroblasts and endothelial cells in synergy with dengue-induced pro-inflammatory mediators. Deposited hyaluronan-rich matrices around cells cultured in vitro recruited CD44-expressing macrophage-like cells, suggesting a mechanism for enhancement of inflammation. In cultured endothelial cells, perturbed hyaluronan-CD44 interactions enhanced endothelial permeability through modulation of VE-cadherin and cytoskeleton re-organization, and exacerbated the NS1-induced disruption of endothelial integrity.

Interpretation: Pharmacological targeting of hyaluronan biosynthesis and/or its CD44-mediated signaling may limit the life-threatening vascular leakiness during moderate-to-severe dengue virus infection. 

Place, publisher, year, edition, pages
ELSEVIER, 2019
Keywords
CD44, Dengue, Hyaluronan, Vascular leakage, VE-cadherin, Cytokines, HAS2, HYAL2, TGEbeta
National Category
Cell and Molecular Biology Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
Identifiers
urn:nbn:se:uu:diva-397776 (URN)10.1016/j.ebiom.2019.09.014 (DOI)000493830800045 ()31526718 (PubMedID)
Funder
Swedish Cancer Society, 2018/337Swedish Cancer Society, 2016/445Swedish Research Council, 2015-02757Academy of Finland
Available from: 2019-11-29 Created: 2019-11-29 Last updated: 2019-11-29Bibliographically approved
Sundqvist, A., Voytyuk, O., Hamdi, M., Popeijus, H. E., Bijlsma-van der Burgt, C., Janssen, J., . . . van Dam, H. (2019). JNK-Dependent cJun Phosphorylation Mitigates TGF beta- and EGF-Induced Pre-Malignant Breast Cancer Cell Invasion by Suppressing AP-1-Mediated Transcriptional Responses. CELLS, 8(12), Article ID 1481.
Open this publication in new window or tab >>JNK-Dependent cJun Phosphorylation Mitigates TGF beta- and EGF-Induced Pre-Malignant Breast Cancer Cell Invasion by Suppressing AP-1-Mediated Transcriptional Responses
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2019 (English)In: CELLS, E-ISSN 2073-4409, Vol. 8, no 12, article id 1481Article in journal (Refereed) Published
Abstract [en]

Transforming growth factor-beta (TGF beta) has both tumor-suppressive and tumor-promoting effects in breast cancer. These functions are partly mediated through Smads, intracellular transcriptional effectors of TGF beta. Smads form complexes with other DNA-binding transcription factors to elicit cell-type-dependent responses. Previously, we found that the collagen invasion and migration of pre-malignant breast cancer cells in response to TGF beta and epidermal growth factor (EGF) critically depend on multiple Jun and Fos components of the activator protein (AP)-1 transcription factor complex. Here we report that the same process is negatively regulated by Jun N-terminal kinase (JNK)-dependent cJun phosphorylation. This was demonstrated by analysis of phospho-deficient, phospho-mimicking, and dimer-specific cJun mutants, and experiments employing a mutant version of the phosphatase MKP1 that specifically inhibits JNK. Hyper-phosphorylation of cJun by JNK strongly inhibited its ability to induce several Jun/Fos-regulated genes and to promote migration and invasion. These results show that MEK-AP-1 and JNK-phospho-cJun exhibit distinct pro- and anti-invasive functions, respectively, through differential regulation of Smad- and AP-1-dependent TGF beta target genes. Our findings are of importance for personalized cancer therapy, such as for patients suffering from specific types of breast tumors with activated EGF receptor-Ras or inactivated JNK pathways.

Place, publisher, year, edition, pages
MDPI, 2019
Keywords
invasion, JNK, cJun, TGF beta, AP-1, MAPK, signaling
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:uu:diva-405350 (URN)10.3390/cells8121481 (DOI)000506643500011 ()31766464 (PubMedID)
Funder
Swedish Cancer Society, 2016/468Swedish Cancer Society, 2015/445Swedish Research Council, 2015-02757EU, European Research Council, 787472
Available from: 2020-02-28 Created: 2020-02-28 Last updated: 2020-02-28Bibliographically approved
Morén, A., Bellomo, C., Tsubakihara, Y., Kardassis, D., Mikulits, W., Heldin, C.-H. & Moustakas, A. (2019). LXR alpha limits TGF beta-dependent hepatocellular carcinoma associated fibroblast differentiation. Oncogenesis, 8, Article ID 36.
Open this publication in new window or tab >>LXR alpha limits TGF beta-dependent hepatocellular carcinoma associated fibroblast differentiation
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2019 (English)In: Oncogenesis, E-ISSN 2157-9024, Vol. 8, article id 36Article in journal (Refereed) Published
Abstract [en]

Transforming growth factor beta (TGF beta) is deposited in the extracellular space of diverse tissues. Resident fibroblasts respond to TGF beta and undergo myofibroblastic differentiation during tissue wound healing and cancer progression. Cancer-associated fibroblasts (CAFs) communicate with tumor cells during cancer progression, under the guidance of TGF beta signaling. We report that agonist-activated liver X receptors (LXR) limit the expression of key components of myofibroblast differentiation, including the a-smooth muscle actin (alpha SMA) gene in liver cancer cells. CAFs derived from hepatocellular carcinoma (HCC) express high aSMA and low LXR alpha levels, whereas hepatocarcinoma cells exhibit an inverse expression pattern. All hepatoma cells analyzed responded to the LXR alpha agonist T0901317 by inducing fatty acid synthase (FASN) expression. On the other hand, T0901317 antagonized TGF beta-induced fibroblastic marker responses, such as fibronectin and calponin, in a subset of hepatoma cells and all CAFs analyzed. Mechanistically, LXR alpha antagonized TGF beta signaling at the transcriptional level. Smad3 and LXR alpha were recruited to adjacent DNA motifs of the ACTA2 promoter. Upon cloning the human ACTA2 promoter, we confirmed its transcriptional induction by TGF beta stimulation, and LXR alpha overexpression repressed the promoter activity. Hepatosphere formation by HCC cells was enhanced upon co-culturing with CAFs. T0901317 suppressed the positive effects exerted on hepatosphere growth by CAFs. Taken together, the data suggest that LXR alpha agonists limit TGF beta-dependent CAF differentiation, potentially limiting primary HCC growth.

National Category
Cancer and Oncology
Identifiers
urn:nbn:se:uu:diva-387277 (URN)10.1038/s41389-019-0140-4 (DOI)000468075200001 ()31097694 (PubMedID)
Funder
Swedish Research Council, K2013-66 x - 14936-10-5Swedish Research Council, 2017-01588Swedish Research Council, 2018-02757Swedish Research Council, 2015-02757EU, FP7, Seventh Framework ProgrammeEU, European Research Council, 787472
Available from: 2019-06-24 Created: 2019-06-24 Last updated: 2019-06-24Bibliographically approved
Morikawa, M., Mitani, Y., Holmborn, K., Kato, T., Koinuma, D., Maruyama, J., . . . Miyazono, K. (2019). The ALK-1/SMAD/ATOH8 axis attenuates hypoxic responses and protects against the development of pulmonary arterial hypertension. Science Signaling, 12(607), Article ID eaay4430.
Open this publication in new window or tab >>The ALK-1/SMAD/ATOH8 axis attenuates hypoxic responses and protects against the development of pulmonary arterial hypertension
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2019 (English)In: Science Signaling, ISSN 1945-0877, E-ISSN 1937-9145, Vol. 12, no 607, article id eaay4430Article in journal (Refereed) Published
Abstract [en]

Dysregulated bone morphogenetic protein (BMP) signaling in endothelial cells (ECs) is implicated in vascular diseases such as pulmonary arterial hypertension (PAH). Here, we showed that the transcription factor ATOH8 was a direct target of SMAD1/5 and was induced in a manner dependent on BMP but independent of Notch, another critical signaling pathway in ECs. In zebrafish and mice, inactivation of Atoh8 did not cause an arteriovenous malformation-like phenotype, which may arise because of dysregulated Notch signaling. In contrast, Atoh8-deficient mice exhibited a phenotype mimicking PAH, which included increased pulmonary arterial pressure and right ventricular hypertrophy. Moreover, ATOH8 expression was decreased in PAH patient lungs. We showed that in cells, ATOH8 interacted with hypoxia-inducible factor 2 alpha (HIF-2 alpha) and decreased its abundance, leading to reduced induction of HIF-2 alpha target genes in response to hypoxia. Together, these findings suggest that the BMP receptor type II/ALK-1/SMAD/ATOH8 axis may attenuate hypoxic responses in ECs in the pulmonary circulation and may help prevent the development of PAH.

Place, publisher, year, edition, pages
American Association for the Advancement of Science, 2019
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-398565 (URN)10.1126/scisignal.aay4430 (DOI)000496799000003 ()31719172 (PubMedID)
Funder
Swedish Cancer Society, 100452Swedish Cancer Society, 2016/445EU, European Research Council, 787472Swedish Research Council, 2015-02757
Available from: 2019-12-09 Created: 2019-12-09 Last updated: 2019-12-09Bibliographically approved
Papoutsoglou, P., Tsubakihara, Y., Caja, L., Morén, A., Pallis, P., Ameur, A., . . . Moustakas, A. (2019). The TGFB2-AS1 lncRNA Regulates TGF-beta Signaling by Modulating Corepressor Activity. Cell reports, 28(12), 3182-3198.ell
Open this publication in new window or tab >>The TGFB2-AS1 lncRNA Regulates TGF-beta Signaling by Modulating Corepressor Activity
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2019 (English)In: Cell reports, ISSN 2211-1247, E-ISSN 2211-1247, Vol. 28, no 12, p. 3182-3198.ellArticle in journal (Refereed) Published
Abstract [en]

Molecular processes involving lncRNAs regulate cell function. By applying transcriptomics, we identify lncRNAs whose expression is regulated by transforming growth factor beta (TGF-beta). Upon silencing individual lncRNAs, we identify several that regulate TGF-beta signaling. Among these lncRNAs, TGFB2-antisense RNA1 (TGFB2-AS1) is induced by TGF-beta through Smad and protein kinase pathways and resides in the nucleus. Depleting TGFB2-AS1 enhances TGF-beta/Smad-mediated transcription and expression of hallmark TGF-beta-target genes. Increased dose of TGFB2-AS1 reduces expression of these genes, attenuates TGF-beta-induced cell growth arrest, and alters BMP and Wnt pathway gene profiles. Mechanistically, TGFB2-AS1, mainly via its 3' terminal region, binds to the EED adaptor of the Polycomb repressor complex 2 (PRC2), promoting repressive histone H3K27me(3) modifications at TGF-beta-target gene promoters. Silencing EED or inhibiting PRC2 methylation activity partially rescues TGFB2-AS1-mediated gene repression. Thus, the TGF-beta-induced TGFB2-AS1 lncRNA exerts inhibitory functions on TGF-beta/BMP signaling output, supporting auto-regulatory negative feedback that balances TGF-beta/BMP-mediated responses.

Place, publisher, year, edition, pages
CELL PRESS, 2019
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-395306 (URN)10.1016/j.celrep.2019.08.028 (DOI)000486389400014 ()31533040 (PubMedID)
Funder
Swedish Cancer Society, CAN2015/438Swedish Research Council, K2013-66X-14936-10-5Swedish Research Council, 2015-02757EU, European Research Council, 787472
Available from: 2019-10-18 Created: 2019-10-18 Last updated: 2019-10-18Bibliographically approved
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Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-9508-896x

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