Colamaio, Marianna
(2010)
miR-191 downregulation plays a role in thyroid follicular tumors through CDK6 targeting.
[Tesi di dottorato]
(Unpublished)
| Item Type: |
Tesi di dottorato
|
| Resource language: |
English |
| Title: |
miR-191 downregulation plays a role in thyroid follicular tumors through CDK6 targeting |
| Creators: |
| Creators | Email |
|---|
| Colamaio, Marianna | marianna.colamaio@virgilio.it |
|
| Date: |
29 November 2010 |
| Number of Pages: |
93 |
| Institution: |
Università degli Studi di Napoli Federico II |
| Department: |
Biologia e patologia cellullare e molecolare "L. Califano" |
| Scuola di dottorato: |
Medicina molecolare |
| Dottorato: |
Genetica e medicina molecolare |
| Ciclo di dottorato: |
23 |
| Coordinatore del Corso di dottorato: |
| nome | email |
|---|
| Nitsch, Lucio | nitsch@unina.it |
|
| Tutor: |
| nome | email |
|---|
| Fusco, Alfredo | UNSPECIFIED | | Battista, Sabrina | UNSPECIFIED |
|
| Date: |
29 November 2010 |
| Number of Pages: |
93 |
| Keywords: |
miR-191, CDK6, thyroid |
| Settori scientifico-disciplinari del MIUR: |
Area 06 - Scienze mediche > MED/03 - Genetica medica
Area 05 - Scienze biologiche > BIO/18 - Genetica |
[error in script]
[error in script]
| Additional information: |
L'attività di dottorato è stata svolta presso l'Istituto di Endocrinologia ed Oncologia Sperimentale (IEOS) del CNR |
| Date Deposited: |
13 Dec 2010 22:30 |
| Last Modified: |
30 Apr 2014 19:45 |
| URI: |
http://www.fedoa.unina.it/id/eprint/8308 |
| DOI: |
10.6092/UNINA/FEDOA/8308 |
Collection description
miR-191 expression is frequently altered in several neoplasias, being
upregulated in some, such as pancreatic, colon, lung and prostate carinomas,
and downregulated in others, such as severe medulloblastomas and melanomas.
I have investigated the expression of miR-191 in thyroid neoplasias.
In my thesis I report that miR-191 is downregulated in follicular adenomas and
carcinomas, with a reduction that is almost 2-fold higher in follicular
carcinomas with respect to adenomas. Conversely it is upregulated in thyroid
carcinomas of the papillary histotype (PTCs), in comparison with the normal
thyroid tissue. Consistent with a putative tumour suppressor role of miR-191 in
the development of thyroid neoplasias of the follicular histotype, functional
studies showed that restoration of miR-191 expression in a follicular thyroid
cancer cell line reduces cell growth and migration rate. Furthermore, I found
that miR-191 negatively regulates the expression of CDK6 protein, involved in
cell cycle control, without changing the CDK6 mRNA level and decreases the
activity of a luciferase reporter construct containing the CDK6-3'untranslated
region. These results demonstrate that miR-191 regulates CDK6 at the posttranscriptional
level, resulting in inhibition of cell proliferation and migration
of the follicular thyroid carcinoma cell line; I will show that restoration of
miR-191 expression reduces cell proliferation leading to an increased number
of the cells in the G1 phase of the cell cycle. Finally, in follicular adenomas
and carcinomas, we immunohistochemically detected CDK6 over-expression,
suggesting that miR-191 may have a pathogenic role in thyroid cancer by
controlling CDK6 expression.
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