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miR-203 is a microRNA that is specifically expressed in keratinocytes (the most abundant cell type in the epidermis) and in normal conditions promotes epidermal differentiation by restricting proliferative potential and inducing cell-cycle exit<ref name="pmid18311128"/>. It does so by repressing p63, an essential regulator of stem cell maintenance in epithelial stratified tissues<ref name="pmid18311128"/>.
miR-203 is a microRNA that is specifically expressed in keratinocytes (the most abundant cell type in the epidermis) and in normal conditions promotes epidermal differentiation by restricting proliferative potential and inducing cell-cycle exit<ref name="pmid18311128"/>. It does so by repressing p63, an essential regulator of stem cell maintenance in epithelial stratified tissues<ref name="pmid18311128"/>.





== Localization ==
== Localization ==
In humans, miR-203 is located in an intergenic region in 14q32.33. In mouse, it is found in chromosome 12[Ensemble].
In humans, miR-203 is located in an intergenic region in 14q32.33. In mouse, it is found in chromosome 12[Ensemble].




== Evidence ==
== Evidence ==
This miRNA was predicted using computational tools by comparison to mouse and tiger blowfish sequences. It has been validated in zebrafish and its expression confirmed in humans<ref name="pmid17604727">{{cite journal |author=Landgraf P, Rusu M, Sheridan R, Sewer A, Iovino N, Aravin A, Pfeffer S, Rice A, Kamphorst AO, Landthaler M, Lin C, Socci ND, Hermida L, Fulci V, Chiaretti S, Foa R, Schliwka J, Fuchs U, Novosel A, Muller RU, Schermer B, Bissels U, Inman J, Phan Q, Chien M |title=A mammalian microRNA expression atlas based on small RNA library sequencing. |journal=Cell |volume=129 |issue=7 |pages=1401-14 |year=2007 |pmid=17604727}}</ref>
This miRNA was predicted using computational tools by comparison to mouse and tiger blowfish sequences. It has been validated in zebrafish and its expression confirmed in humans<ref name="pmid17604727">{{cite journal |author=Landgraf P, Rusu M, Sheridan R, Sewer A, Iovino N, Aravin A, Pfeffer S, Rice A, Kamphorst AO, Landthaler M, Lin C, Socci ND, Hermida L, Fulci V, Chiaretti S, Foa R, Schliwka J, Fuchs U, Novosel A, Muller RU, Schermer B, Bissels U, Inman J, Phan Q, Chien M |title=A mammalian microRNA expression atlas based on small RNA library sequencing. |journal=Cell |volume=129 |issue=7 |pages=1401-14 |year=2007 |pmid=17604727}}</ref>
[7].
[7].




== Targets ==
== Targets ==
Line 39: Line 44:
There is some controversy as to whether SOCS3 (suppressor of cytokine signaling 3) is also targeted by miR-203. In their study, AM Lena et al. (2008)<ref name="pmid18483491">{{cite journal |author=Lena AM, Shalom-Feuerstein R, Rivetti di Val Cervo P, Aberdam D, Knight RA, Melino G, Candi E |title=miR-203 represses 'stemness' by repressing DeltaNp63. |journal=Cell Death Differ |volume=15 |issue=7 |pages=1187-95 |year=2008 |pmid=18483491}}</ref> showed that, despite bioinformatic alignment of miR-203 with SOCS3 3'UTR, the levels of SOCS3 transcripts increased in keratinocytes stimulated to differentiate in vitro, in parallel with miR-203. Then they exogenously expressed miR-203 in mouse keratinocytes and showed that SOCS3 is not repressed by miR-203.
There is some controversy as to whether SOCS3 (suppressor of cytokine signaling 3) is also targeted by miR-203. In their study, AM Lena et al. (2008)<ref name="pmid18483491">{{cite journal |author=Lena AM, Shalom-Feuerstein R, Rivetti di Val Cervo P, Aberdam D, Knight RA, Melino G, Candi E |title=miR-203 represses 'stemness' by repressing DeltaNp63. |journal=Cell Death Differ |volume=15 |issue=7 |pages=1187-95 |year=2008 |pmid=18483491}}</ref> showed that, despite bioinformatic alignment of miR-203 with SOCS3 3'UTR, the levels of SOCS3 transcripts increased in keratinocytes stimulated to differentiate in vitro, in parallel with miR-203. Then they exogenously expressed miR-203 in mouse keratinocytes and showed that SOCS3 is not repressed by miR-203.


In contrast, T Wei et al. (2010)<ref name="pmid20698882"/> validated SOCS3 as a target for miR-203. In their study, they introduced the SOCS3 3'UTR fragment encompassing the putative target site in a luciferase reporter vector, and they observed a significant decrease in luciferase activity when miR-203 was introduced compared to controls. They also generated a mutation in the binding site and reported restoration of luciferase activity, as well as mutually exclusive localization with miR-203. They concluded that SOCS3 is targeted by miR-203, and hypothesize that miR-203 regulation of SOCS3 and thus of Stat3 could have implications in keratinocyte functions.
In contrast, T Wei et al. (2010)<ref name="pmid20698882"/> validated SOCS3 as a target for miR-203. In their study, they introduced the SOCS3 3'UTR fragment encompassing the putative target site in a luciferase reporter vector, and they observed a significant decrease in luciferase activity when miR-203 was introduced compared to controls. They also generated a mutation in the binding site and reported restoration of luciferase activity, as well as mutually exclusive localization with miR-203. They concluded that SOCS3 is targeted by miR-203, and hypothesize that miR-203 regulation of SOCS3 and thus of Stat3 could have implications in keratinocyte functions.

⚫
Another putative target is ABL1, which is found activated in hematopoietic malignancies where miR-203 is epigenetically silenced by hypermethylation<ref name="pmid18538733">{{cite journal |author=Bueno MJ, Pérez de Castro I, Gómez de Cedrón M, Santos J, Calin GA, Cigudosa JC, Croce CM, Fernández-Piqueras J, Malumbres M |title=Genetic and epigenetic silencing of microRNA-203 enhances ABL1 and BCR-ABL1 oncogene expression. |journal=Cancer Cell |volume=13 |issue=6 |pages=496-506 |year=2008 |pmid=18538733}}</ref>.




== Foetal skin development ==
== Foetal skin development ==
Yi R et al. showed that in mice, the expression of miR-203 is significantly upregulated between E13.5 and E15.5, suggesting that it may be absent from multipotent progenitors of single-layered epidermis, but is induced upon stratification and differentiation<ref name="pmid18311128"/>. It also was expressed at high levels in differentiating cells such as hair follicles, epidermis and sebaceous glands.
Yi R et al. showed that in mice, the expression of miR-203 is significantly upregulated between E13.5 and E15.5, suggesting that it may be absent from multipotent progenitors of single-layered epidermis, but is induced upon stratification and differentiation<ref name="pmid18311128"/>. It also was expressed at high levels in differentiating cells such as hair follicles, epidermis and sebaceous glands.
A study by Wei T et al. demonstrated that in humans, miR-203 expression is first detectable at 17 weeks gestation in the suprabasal layers of epidermis, and this localization was conserved in the adult skin<ref name="pmid20698882">{{cite journal |author=Wei T, Orfanidis K, Xu N, Janson P, Ståhle M, Pivarcsi A, Sonkoly E |title=The expression of microRNA-203 during human skin morphogenesis. |journal=Exp Dermatol |volume=19 |issue=9 |pages=854-6 |year=2010 |pmid=20698882}}</ref>.
Wei T et al.<ref name="pmid20698882">{{cite journal |author=Wei T, Orfanidis K, Xu N, Janson P, Ståhle M, Pivarcsi A, Sonkoly E |title=The expression of microRNA-203 during human skin morphogenesis. |journal=Exp Dermatol |volume=19 |issue=9 |pages=854-6 |year=2010 |pmid=20698882}}</ref> demonstrated that in humans, miR-203 expression is first detectable at 17 weeks gestation in the suprabasal layers of epidermis, and this localization was conserved in the adult skin. When miR-203 is expressed prematurely, basal cells diminish their proliferative potential; and when it is absent, proliferation is no longer restricted to the basal layer of epidermis<ref name="pmid19209183">{{cite journal |author=Blanpain C, Fuchs E |title=Epidermal homeostasis: a balancing act of stem cells in the skin. |journal=Nat Rev Mol Cell Biol. |volume=10 |issue=3 |pages=207-17 |year=2009 |pmid=19209183}}</ref>.




== Role in carcinogenesis ==
== Role in carcinogenesis ==
miR-203 has been found overexpressed in pancreatic adenocarcinoma and shows correlation with poor prognosis in patients that had underwent pancreatectomy, and has been suggested as a new prognostic marker for this disease <ref name="pmid20652642"/><ref name="pmid19551852">{{cite journal |author=Greither T, Grochola LF, Udelnow A, Lautenschläger C, Würl P, Taubert H |title=Elevated expression of microRNAs 155, 203, 210 and 222 in pancreatic tumors is associated with poorer survival. |journal=Int J Cancer |volume=126 |issue=1 |pages=73-80 |year=2010 |pmid=19551852}}</ref>. Also, miR-203 has been identified as target of human papillomavirus (HPV) protein E7<ref name="pmid20219920"/>, which causes its downregulation and thus de-repression of p63 and its downstream targets, ensuring proliferative potential on the host cell, required for the virus to replicate. High levels of miR-203 are inhibitory of HPV amplification<ref name="pmid20219920"/>.
miR-203 has been found overexpressed in pancreatic adenocarcinoma and shows correlation with poor prognosis in patients that had underwent pancreatectomy, and has been suggested as a new prognostic marker for this disease <ref name="pmid20652642"/><ref name="pmid19551852">{{cite journal |author=Greither T, Grochola LF, Udelnow A, Lautenschläger C, Würl P, Taubert H |title=Elevated expression of microRNAs 155, 203, 210 and 222 in pancreatic tumors is associated with poorer survival. |journal=Int J Cancer |volume=126 |issue=1 |pages=73-80 |year=2010 |pmid=19551852}}</ref>. Also, miR-203 has been identified as target of human papillomavirus (HPV) protein E7<ref name="pmid20219920"/>, which causes its downregulation and thus de-repression of p63 and its downstream targets, ensuring proliferative potential on the host cell, required for the virus to replicate. High levels of miR-203 are inhibitory of HPV amplification<ref name="pmid20219920"/>.

miR-203 has also been proposed as a tumour-suppresive microRNA in hepatocellular carcinoma (HCC). In their study, Furuta M et al.<ref name="pmid19843643">{{cite journal |author=Furuta M, Kozaki KI, Tanaka S, Arii S, Imoto I, Inazawa J |title=miR-124 and miR-203 are epigenetically silenced tumor-suppressive microRNAs in hepatocellular carcinoma. |journal=Carcinogenesis |volume=31 |issue=5 |pages=766-76 |year=2010 |pmid=19843643}}</ref> found miR-203, along with miR-124, epigenetically silenced in primary HCC tumours compared with non-tumorous liver tissues. Also, expression of miR-203 in HCC cells lacking their expression inhibited cell growth and downregulated a set of other possible targets.
miR-203 has also been proposed as a tumour-suppresive microRNA in hepatocellular carcinoma (HCC) and hematopoietic malignancies. In their study, Furuta M et al.<ref name="pmid19843643">{{cite journal |author=Furuta M, Kozaki KI, Tanaka S, Arii S, Imoto I, Inazawa J |title=miR-124 and miR-203 are epigenetically silenced tumor-suppressive microRNAs in hepatocellular carcinoma. |journal=Carcinogenesis |volume=31 |issue=5 |pages=766-76 |year=2010 |pmid=19843643}}</ref> found miR-203, along with miR-124, epigenetically silenced in primary HCC tumours compared with non-tumorous liver tissues. Also, expression of miR-203 in HCC cells lacking their expression inhibited cell growth and downregulated a set of other possible targets. Bueno MJ et al.<ref name="pmid18538733"/> also found silencing of miR-203 in some leukemias, as well as an inverse correlation between miR-203 and ABL1 levels (sometimes expressed as the BCR-ABL1 fusion protein). Supporting its role as a tumour suppresor, it has also been found upregulated upon UVC irradiation in the squamous cell carcinoma lines, suggesting a connection between miR-203 and the activation of the apoptotic program<ref name="pmid18483491"/>.





== Role in psoriasis ==
== Role in psoriasis ==
Sonkoly E et al.<ref name="pmid17622355">{{cite journal |author=Sonkoly E, Wei T, Janson PC, Sääf A, Lundeberg L, Tengvall-Linder M, Norstedt G, Alenius H, Homey B, Scheynius A, Ståhle M, Pivarcsi A |title=MicroRNAs: novel regulators involved in the pathogenesis of psoriasis? |journal=PLoS One |volume=2 |issue=7 |pages=e610 |year=2007 |pmid=17622355}}</ref> identified miR-203 as a psoriasis-specific microRNA when compared with healthy human skin or atopic eczema, and observed downregulation of SOCS3 concurrently with upregulation of miR-203 in psoriatic plaques, potentially having an effect in inflammatory responses.


== See also ==
== See also ==
Line 64: Line 78:
<ref name="pmid20702634">{{cite journal |author=McKenna DJ, McDade SS, Patel D, McCance DJ |title=MicroRNA 203 expression in keratinocytes is dependent on regulation of p53 levels by E6. |journal=J Virol |volume=84 |issue=20 |pages=10644-52 |year=2010 |pmid=20702634}}</ref>
<ref name="pmid20702634">{{cite journal |author=McKenna DJ, McDade SS, Patel D, McCance DJ |title=MicroRNA 203 expression in keratinocytes is dependent on regulation of p53 levels by E6. |journal=J Virol |volume=84 |issue=20 |pages=10644-52 |year=2010 |pmid=20702634}}</ref>
<ref name="pmid19759552">{{cite journal |author=Sonkoly E, Wei T, Pavez Loriè E, Suzuki H, Kato M, Törmä H, Ståhle M, Pivarcsi A |title=Protein kinase C-dependent upregulation of miR-203 induces the differentiation of human keratinocytes. |journal=J Invest Dermatol |volume=130 |issue=1 |pages=124-34 |year=2010 |pmid=19759552}}</ref>
<ref name="pmid19759552">{{cite journal |author=Sonkoly E, Wei T, Pavez Loriè E, Suzuki H, Kato M, Törmä H, Ståhle M, Pivarcsi A |title=Protein kinase C-dependent upregulation of miR-203 induces the differentiation of human keratinocytes. |journal=J Invest Dermatol |volume=130 |issue=1 |pages=124-34 |year=2010 |pmid=19759552}}</ref>

⚫
<ref name="pmid18538733">{{cite journal |author=Bueno MJ, Pérez de Castro I, Gómez de Cedrón M, Santos J, Calin GA, Cigudosa JC, Croce CM, Fernández-Piqueras J, Malumbres M |title=Genetic and epigenetic silencing of microRNA-203 enhances ABL1 and BCR-ABL1 oncogene expression. |journal=Cancer Cell |volume=13 |issue=6 |pages=496-506 |year=2008 |pmid=18538733}}</ref>
<ref name="pmid20885409">{{cite journal |author=Garzon R, Marcucci G, Croce CM |title=Targeting microRNAs in cancer: rationale, strategies and challenges. |journal=Nat Rev Drug Discov. |volume=9 |issue=10 |pages=775-89 |year=2010 |pmid=20885409}}</ref>


</div>
</div>

Revision as of 00:00, 9 November 2010

mir-203
miR-203 microRNA secondary structure and sequence conservation
Identifiers
Symbolmir-203
RfamRF00696
miRBase familyMIPF0000108
NCBI Gene406986
HGNC31581
OMIM611899
Other data
RNA typemicroRNA
Domain(s)Eukaryota; Euteleostomi
PDB structuresPDBe

In molecular biology mir-203 microRNA is a short non-coding RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms, such as translational repression and Argonaute-catalyzed mRNA cleavage[1][2]. miR-203 has been identified as a skin-specific miRNA, and it forms an expression gradient that defines the boundary between proliferative epidermal basal progenitors and terminally differentiating suprabasal cells[3]. It has also been found upregulated in psoriasis[4] and differentially expressed in some types of cancer[5][6].

Introduction

MicroRNAs are short (20-22nt), non-coding RNA molecules involved in the regulation of messenger RNAs (mRNAs) by pairing with their 3’ UTR and affecting their stability[4] or directing their silencing or degradation[1]. MicroRNAs are likely to play roles in most cellular processes, including proliferation, development, differentiation and apoptosis[5]. They are located in intergenic and intragenic regions, and are transcribed as pri-miRNA by Pol II or Pol III[4]. They then undergo extensive post-transcriptional modifications, starting with the processing of the pri-miRNA in the nucleus to generate a 70-100 nt long pre-miRNA by ribonucleases Drosha and DGCR8. This pre-miRNA is then transported out of the nucleus by Exportin-5, and is then further processed by Dicer into a mature 18-25 nt long double stranded microRNA[7]. The guide strand of the miRNA is then loaded into RISC (RNA-inducing silencing complex)[7] and is then able to pair with its target. The passenger strand, denoted by a star, is commonly degraded, though this is not always the case[8].

miR-203 is a microRNA that is specifically expressed in keratinocytes (the most abundant cell type in the epidermis) and in normal conditions promotes epidermal differentiation by restricting proliferative potential and inducing cell-cycle exit[3]. It does so by repressing p63, an essential regulator of stem cell maintenance in epithelial stratified tissues[3].


Localization

In humans, miR-203 is located in an intergenic region in 14q32.33. In mouse, it is found in chromosome 12[Ensemble].


Evidence

This miRNA was predicted using computational tools by comparison to mouse and tiger blowfish sequences. It has been validated in zebrafish and its expression confirmed in humans[9] [7].


Targets

miR-203 has one validated target, p63, conserved across vertebrate lineages. p63 is an essential regulator of stem cell maintenance in stratified epithelial tissues. Yi R et al.[3] confirmed p63 as a target of miR-203. They showed that miR-203 expression is conspicuous in terminally differentiating epithelial cells, but is not present on their proliferative progenitor compartments, and shows a mutually exclusive pattern of expression with p63. They also report downregulation of proteins downstream of p63, suggesting a mechanistic method for inhibition of proliferative potential of epidermal stem cells.

There is some controversy as to whether SOCS3 (suppressor of cytokine signaling 3) is also targeted by miR-203. In their study, AM Lena et al. (2008)[10] showed that, despite bioinformatic alignment of miR-203 with SOCS3 3'UTR, the levels of SOCS3 transcripts increased in keratinocytes stimulated to differentiate in vitro, in parallel with miR-203. Then they exogenously expressed miR-203 in mouse keratinocytes and showed that SOCS3 is not repressed by miR-203.

In contrast, T Wei et al. (2010)[11] validated SOCS3 as a target for miR-203. In their study, they introduced the SOCS3 3'UTR fragment encompassing the putative target site in a luciferase reporter vector, and they observed a significant decrease in luciferase activity when miR-203 was introduced compared to controls. They also generated a mutation in the binding site and reported restoration of luciferase activity, as well as mutually exclusive localization with miR-203. They concluded that SOCS3 is targeted by miR-203, and hypothesize that miR-203 regulation of SOCS3 and thus of Stat3 could have implications in keratinocyte functions.

Another putative target is ABL1, which is found activated in hematopoietic malignancies where miR-203 is epigenetically silenced by hypermethylation[12].


Foetal skin development

Yi R et al. showed that in mice, the expression of miR-203 is significantly upregulated between E13.5 and E15.5, suggesting that it may be absent from multipotent progenitors of single-layered epidermis, but is induced upon stratification and differentiation[3]. It also was expressed at high levels in differentiating cells such as hair follicles, epidermis and sebaceous glands.

Wei T et al.[11] demonstrated that in humans, miR-203 expression is first detectable at 17 weeks gestation in the suprabasal layers of epidermis, and this localization was conserved in the adult skin. When miR-203 is expressed prematurely, basal cells diminish their proliferative potential; and when it is absent, proliferation is no longer restricted to the basal layer of epidermis[13].


Role in carcinogenesis

miR-203 has been found overexpressed in pancreatic adenocarcinoma and shows correlation with poor prognosis in patients that had underwent pancreatectomy, and has been suggested as a new prognostic marker for this disease [5][14]. Also, miR-203 has been identified as target of human papillomavirus (HPV) protein E7[6], which causes its downregulation and thus de-repression of p63 and its downstream targets, ensuring proliferative potential on the host cell, required for the virus to replicate. High levels of miR-203 are inhibitory of HPV amplification[6].

miR-203 has also been proposed as a tumour-suppresive microRNA in hepatocellular carcinoma (HCC) and hematopoietic malignancies. In their study, Furuta M et al.[15] found miR-203, along with miR-124, epigenetically silenced in primary HCC tumours compared with non-tumorous liver tissues. Also, expression of miR-203 in HCC cells lacking their expression inhibited cell growth and downregulated a set of other possible targets. Bueno MJ et al.[12] also found silencing of miR-203 in some leukemias, as well as an inverse correlation between miR-203 and ABL1 levels (sometimes expressed as the BCR-ABL1 fusion protein). Supporting its role as a tumour suppresor, it has also been found upregulated upon UVC irradiation in the squamous cell carcinoma lines, suggesting a connection between miR-203 and the activation of the apoptotic program[10].


Role in psoriasis

Sonkoly E et al.[16] identified miR-203 as a psoriasis-specific microRNA when compared with healthy human skin or atopic eczema, and observed downregulation of SOCS3 concurrently with upregulation of miR-203 in psoriatic plaques, potentially having an effect in inflammatory responses.

See also

References

  1. ^ a b Bartel DP (2009). "MicroRNAs: target recognition and regulatory functions". Cell. 136 (2): 215–33. PMID 19167326.
  2. ^ Bartel DP (2004). "MicroRNAs: genomics, biogenesis, mechanism, and function". Cell. 116 (2): 281–97. PMID 14744438.
  3. ^ a b c d e Yi R, Poy MN, Stoffel M, Fuchs E (2008). "A skin microRNA promotes differentiation by repressing 'stemness'". Nature. 452 (7184): 225–9. PMID 18311128.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  4. ^ a b c Bostjancic E, Glavac D (2008). "Importance of microRNAs in skin morphogenesis and diseases". Acta Dermatovenerol Alp Panonica Adriat. 17 (3): 95–102. PMID 18853072.
  5. ^ a b c Ikenaga N, Ohuchida K, Mizumoto K, Yu J, Kayashima T, Sakai H, Fujita H, Nakata K, Tanaka M (2010). "MicroRNA-203 Expression as a New Prognostic Marker of Pancreatic Adenocarcinoma". Ann Surg Oncol. PMID 20652642.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  6. ^ a b c Melar-New M, Laimins LA (2010). "Human papillomaviruses modulate expression of microRNA 203 upon epithelial differentiation to control levels of p63 proteins". J Virol. 84 (10): 5212–21. PMID 20219920.
  7. ^ a b Garzon R, Marcucci G, Croce CM (2010). "Targeting microRNAs in cancer: rationale, strategies and challenges". Nat Rev Drug Discov. 9 (10): 775–89. PMID 20885409.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  8. ^ Guo L, Lu Z (2010). "The fate of miRNA* strand through evolutionary analysis: implication for degradation as merely carrier strand or potential regulatory molecule?". PLoS One. 5 (6): e11387. PMID 20613982.
  9. ^ Landgraf P, Rusu M, Sheridan R, Sewer A, Iovino N, Aravin A, Pfeffer S, Rice A, Kamphorst AO, Landthaler M, Lin C, Socci ND, Hermida L, Fulci V, Chiaretti S, Foa R, Schliwka J, Fuchs U, Novosel A, Muller RU, Schermer B, Bissels U, Inman J, Phan Q, Chien M (2007). "A mammalian microRNA expression atlas based on small RNA library sequencing". Cell. 129 (7): 1401–14. PMID 17604727.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  10. ^ a b Lena AM, Shalom-Feuerstein R, Rivetti di Val Cervo P, Aberdam D, Knight RA, Melino G, Candi E (2008). "miR-203 represses 'stemness' by repressing DeltaNp63". Cell Death Differ. 15 (7): 1187–95. PMID 18483491.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  11. ^ a b Wei T, Orfanidis K, Xu N, Janson P, StÃ¥hle M, Pivarcsi A, Sonkoly E (2010). "The expression of microRNA-203 during human skin morphogenesis". Exp Dermatol. 19 (9): 854–6. PMID 20698882.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  12. ^ a b Bueno MJ, Pérez de Castro I, Gómez de Cedrón M, Santos J, Calin GA, Cigudosa JC, Croce CM, Fernández-Piqueras J, Malumbres M (2008). "Genetic and epigenetic silencing of microRNA-203 enhances ABL1 and BCR-ABL1 oncogene expression". Cancer Cell. 13 (6): 496–506. PMID 18538733.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  13. ^ Blanpain C, Fuchs E (2009). "Epidermal homeostasis: a balancing act of stem cells in the skin". Nat Rev Mol Cell Biol. 10 (3): 207–17. PMID 19209183.
  14. ^ Greither T, Grochola LF, Udelnow A, Lautenschläger C, Würl P, Taubert H (2010). "Elevated expression of microRNAs 155, 203, 210 and 222 in pancreatic tumors is associated with poorer survival". Int J Cancer. 126 (1): 73–80. PMID 19551852.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  15. ^ Furuta M, Kozaki KI, Tanaka S, Arii S, Imoto I, Inazawa J (2010). "miR-124 and miR-203 are epigenetically silenced tumor-suppressive microRNAs in hepatocellular carcinoma". Carcinogenesis. 31 (5): 766–76. PMID 19843643.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  16. ^ Sonkoly E, Wei T, Janson PC, Sääf A, Lundeberg L, Tengvall-Linder M, Norstedt G, Alenius H, Homey B, Scheynius A, Ståhle M, Pivarcsi A (2007). "MicroRNAs: novel regulators involved in the pathogenesis of psoriasis?". PLoS One. 2 (7): e610. PMID 17622355.{{cite journal}}: CS1 maint: multiple names: authors list (link)

Further reading

  1. ^ Stanczyk J, Ospelt C, Karouzakis E, Filer A, Raza K, Kolling C, Gay R, Buckley CD, Tak PP, Gay S, Kyburz D (2010). "Altered expression of miR-203 in rheumatoid arthritis synovial fibroblasts and its role in fibroblast activation". Arthritis Rheum. PMID 20981815.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  2. ^ McKenna DJ, McDade SS, Patel D, McCance DJ (2010). "MicroRNA 203 expression in keratinocytes is dependent on regulation of p53 levels by E6". J Virol. 84 (20): 10644–52. PMID 20702634.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  3. ^ Sonkoly E, Wei T, Pavez Loriè E, Suzuki H, Kato M, Törmä H, StÃ¥hle M, Pivarcsi A (2010). "Protein kinase C-dependent upregulation of miR-203 induces the differentiation of human keratinocytes". J Invest Dermatol. 130 (1): 124–34. PMID 19759552.{{cite journal}}: CS1 maint: multiple names: authors list (link)

External links

Retrieved from "https://en.wikipedia.org/w/index.php?title=MiR-203&oldid=395641181"