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miR-19a/b modulates lung cancer cells metastasis through suppression of MXD1 expression

View Article: PubMed Central - PubMed

ABSTRACT

Increasing evidence has shown that microRNA (miRNA) is extensively involved in the pathophysiology of lung cancer. Microarray data demonstrated the increasing levels of miR-19a in the peripheral blood from patients suffering from lung cancer, which is closely associated with poor prognosis of lung cancer. However, the underlying molecular mechanism of miR-19a remains to be determined. The results of the present study showed a higher expression of miR-19a compared with normal bronchial epithelial cells. Furthermore, lentivirus vectors were constructed to establish cell lines that overexpressed and knocked out miR-19a in order to study the role of miR-19a on the metastasis and proliferation of lung cancer cells. Investigation into the underlying mechanism of miR-19a, revealed that MXD1 may be the key gene targeting miR-19a, participating in the process of proliferation and metastasis of lung cancer cells.

No MeSH data available.


Expression of MXD1 at the gene and protein level. Suffix of ‘a’ indicates an overexpression of miR-19a while suffix of ‘I’ indicating a knockdown of miR-19a (***P<0.001).
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f6-ol-0-0-4881: Expression of MXD1 at the gene and protein level. Suffix of ‘a’ indicates an overexpression of miR-19a while suffix of ‘I’ indicating a knockdown of miR-19a (***P<0.001).

Mentions: MXD1 was capable of binding with MAX competitively, which inhibited the formation of the c-Myc/MAX heterodimers, and the transcriptional activity of c-Myc was downregulated (16). Our results found that following the overexpression of miR-19a in cancer cells, MXD1 expression was significantly downregulated, which indicated that miR-19a may regulate MXD1 expression negatively, and thus promote the formation of c-myc/max heterodimers indirectly, thereby enhancing cell proliferation. (Fig. 6).


miR-19a/b modulates lung cancer cells metastasis through suppression of MXD1 expression
Expression of MXD1 at the gene and protein level. Suffix of ‘a’ indicates an overexpression of miR-19a while suffix of ‘I’ indicating a knockdown of miR-19a (***P<0.001).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4998008&req=5

f6-ol-0-0-4881: Expression of MXD1 at the gene and protein level. Suffix of ‘a’ indicates an overexpression of miR-19a while suffix of ‘I’ indicating a knockdown of miR-19a (***P<0.001).
Mentions: MXD1 was capable of binding with MAX competitively, which inhibited the formation of the c-Myc/MAX heterodimers, and the transcriptional activity of c-Myc was downregulated (16). Our results found that following the overexpression of miR-19a in cancer cells, MXD1 expression was significantly downregulated, which indicated that miR-19a may regulate MXD1 expression negatively, and thus promote the formation of c-myc/max heterodimers indirectly, thereby enhancing cell proliferation. (Fig. 6).

View Article: PubMed Central - PubMed

ABSTRACT

Increasing evidence has shown that microRNA (miRNA) is extensively involved in the pathophysiology of lung cancer. Microarray data demonstrated the increasing levels of miR-19a in the peripheral blood from patients suffering from lung cancer, which is closely associated with poor prognosis of lung cancer. However, the underlying molecular mechanism of miR-19a remains to be determined. The results of the present study showed a higher expression of miR-19a compared with normal bronchial epithelial cells. Furthermore, lentivirus vectors were constructed to establish cell lines that overexpressed and knocked out miR-19a in order to study the role of miR-19a on the metastasis and proliferation of lung cancer cells. Investigation into the underlying mechanism of miR-19a, revealed that MXD1 may be the key gene targeting miR-19a, participating in the process of proliferation and metastasis of lung cancer cells.

No MeSH data available.