Limits...
Implications of miR cluster 143/145 as universal anti-oncomiRs and their dysregulation during tumorigenesis.

Das AV, Pillai RM - Cancer Cell Int. (2015)

Bottom Line: Tumorigenesis is a multistep process, de-regulated due to the imbalance of oncogenes as well as anti-oncogenes, resulting in disruption of tissue homeostasis.In many cases the effect of oncogenes and anti-oncogenes are mediated by various other molecules such as microRNAs. microRNAs are small non-coding RNAs established to post-transcriptionally regulate more than half of the protein coding genes. miR cluster 143/145 is one such cancer-related microRNA cluster which is down-regulated in most of the cancers and is able to hinder tumorigenesis by targeting tumor-associated genes.Their low levels precede events which lead to cancer progression and therefore could be considered also as biomarkers to stage the disease.

View Article: PubMed Central - PubMed

Affiliation: Cancer Research Program-9, Rajiv Gandhi Centre for Biotechnology, Thycaud.P.O., Thiruvananthapuram-14, Kerala India.

ABSTRACT
Tumorigenesis is a multistep process, de-regulated due to the imbalance of oncogenes as well as anti-oncogenes, resulting in disruption of tissue homeostasis. In many cases the effect of oncogenes and anti-oncogenes are mediated by various other molecules such as microRNAs. microRNAs are small non-coding RNAs established to post-transcriptionally regulate more than half of the protein coding genes. miR cluster 143/145 is one such cancer-related microRNA cluster which is down-regulated in most of the cancers and is able to hinder tumorigenesis by targeting tumor-associated genes. The fact that they could sensitize drug-resistant cancer cells by targeting multidrug resistant genes makes them potent tools to target cancer cells. Their low levels precede events which lead to cancer progression and therefore could be considered also as biomarkers to stage the disease. Interestingly, evidence suggests the existence of several in vivo mechanisms by which this cluster is differentially regulated at the molecular level to keep their levels low in cancer. In this review, we summarize the roles of miR cluster 143/145 in cancer, their potential prognostic applications and also their regulation during tumorigenesis.

No MeSH data available.


Related in: MedlinePlus

miR cluster 143/145 is evolutionarily conserved across species. a Schematic of chromosomal location of miR cluster 143/145 (adapted from UCSC genome browser. b Schematic representation of structures of miR cluster 143/145 primary transcripts and their location. Multi-species alignment of sequences of miR-143 (c) and miR-145 (d) (courtesy to Clustal W Omega)
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
getmorefigures.php?uid=PMC4588501&req=5

Fig1: miR cluster 143/145 is evolutionarily conserved across species. a Schematic of chromosomal location of miR cluster 143/145 (adapted from UCSC genome browser. b Schematic representation of structures of miR cluster 143/145 primary transcripts and their location. Multi-species alignment of sequences of miR-143 (c) and miR-145 (d) (courtesy to Clustal W Omega)

Mentions: miR cluster 143/145 comprises of two miRNAs, miR-143 and miR-145, that have significant roles in various cellular functions and are co-expressed in a variety of cell types and tissues [28]. These miRNAs are transcribed from a putative cluster on chromosome 5 in human (5q33) and chromosome 18 in mouse (18qE1), and are conserved across species (Fig. 1). miR-143 is separated from miR-145 by ~1.7 kb sequence [28]. Since they are in the same cluster and suggested to be transcribed together, it was speculated that they could be involved in similar functions. However, independent involvement of these miRNAs is also reported in many cellular processes. Both miR-143 and miR-145 are expressed in normal tissues in significant levels, with highest expression in colon and lowest in liver and brain [28]. The expression of these miRNAs was considerably high in prostate, cervix, stomach, uterus and small intestine and low in kidney, placenta, testis, spleen and skeletal muscle [28]. This cluster is found enriched in embryonic stem cells which differentiate into cardiac progenitors [29] suggesting an involvement in cardiac morphogenesis. They play a very important role in the fate specification of vascular smooth muscle cells since they target a number of transcription factors to inhibit proliferation in order to promote differentiation [29].Fig. 1


Implications of miR cluster 143/145 as universal anti-oncomiRs and their dysregulation during tumorigenesis.

Das AV, Pillai RM - Cancer Cell Int. (2015)

miR cluster 143/145 is evolutionarily conserved across species. a Schematic of chromosomal location of miR cluster 143/145 (adapted from UCSC genome browser. b Schematic representation of structures of miR cluster 143/145 primary transcripts and their location. Multi-species alignment of sequences of miR-143 (c) and miR-145 (d) (courtesy to Clustal W Omega)
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4588501&req=5

Fig1: miR cluster 143/145 is evolutionarily conserved across species. a Schematic of chromosomal location of miR cluster 143/145 (adapted from UCSC genome browser. b Schematic representation of structures of miR cluster 143/145 primary transcripts and their location. Multi-species alignment of sequences of miR-143 (c) and miR-145 (d) (courtesy to Clustal W Omega)
Mentions: miR cluster 143/145 comprises of two miRNAs, miR-143 and miR-145, that have significant roles in various cellular functions and are co-expressed in a variety of cell types and tissues [28]. These miRNAs are transcribed from a putative cluster on chromosome 5 in human (5q33) and chromosome 18 in mouse (18qE1), and are conserved across species (Fig. 1). miR-143 is separated from miR-145 by ~1.7 kb sequence [28]. Since they are in the same cluster and suggested to be transcribed together, it was speculated that they could be involved in similar functions. However, independent involvement of these miRNAs is also reported in many cellular processes. Both miR-143 and miR-145 are expressed in normal tissues in significant levels, with highest expression in colon and lowest in liver and brain [28]. The expression of these miRNAs was considerably high in prostate, cervix, stomach, uterus and small intestine and low in kidney, placenta, testis, spleen and skeletal muscle [28]. This cluster is found enriched in embryonic stem cells which differentiate into cardiac progenitors [29] suggesting an involvement in cardiac morphogenesis. They play a very important role in the fate specification of vascular smooth muscle cells since they target a number of transcription factors to inhibit proliferation in order to promote differentiation [29].Fig. 1

Bottom Line: Tumorigenesis is a multistep process, de-regulated due to the imbalance of oncogenes as well as anti-oncogenes, resulting in disruption of tissue homeostasis.In many cases the effect of oncogenes and anti-oncogenes are mediated by various other molecules such as microRNAs. microRNAs are small non-coding RNAs established to post-transcriptionally regulate more than half of the protein coding genes. miR cluster 143/145 is one such cancer-related microRNA cluster which is down-regulated in most of the cancers and is able to hinder tumorigenesis by targeting tumor-associated genes.Their low levels precede events which lead to cancer progression and therefore could be considered also as biomarkers to stage the disease.

View Article: PubMed Central - PubMed

Affiliation: Cancer Research Program-9, Rajiv Gandhi Centre for Biotechnology, Thycaud.P.O., Thiruvananthapuram-14, Kerala India.

ABSTRACT
Tumorigenesis is a multistep process, de-regulated due to the imbalance of oncogenes as well as anti-oncogenes, resulting in disruption of tissue homeostasis. In many cases the effect of oncogenes and anti-oncogenes are mediated by various other molecules such as microRNAs. microRNAs are small non-coding RNAs established to post-transcriptionally regulate more than half of the protein coding genes. miR cluster 143/145 is one such cancer-related microRNA cluster which is down-regulated in most of the cancers and is able to hinder tumorigenesis by targeting tumor-associated genes. The fact that they could sensitize drug-resistant cancer cells by targeting multidrug resistant genes makes them potent tools to target cancer cells. Their low levels precede events which lead to cancer progression and therefore could be considered also as biomarkers to stage the disease. Interestingly, evidence suggests the existence of several in vivo mechanisms by which this cluster is differentially regulated at the molecular level to keep their levels low in cancer. In this review, we summarize the roles of miR cluster 143/145 in cancer, their potential prognostic applications and also their regulation during tumorigenesis.

No MeSH data available.


Related in: MedlinePlus