Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P04637 (
p53
)
77,613
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
In our previous study, we identified an association of high expression of c3orf1, also known as TIMMDC1 (translocase of inner mitochondrial membrane domain-containing protein 1), with metastatic characteristics in lung carcinoma cells. To investigate the preliminary function and mechanism of this mitochondrial protein, we depleted
C3orf1
expression by introducing siRNA into 95D lung carcinoma cells. We demonstrated that
C3orf1
depletion significantly suppressed 95D cell growth and migration. We confirmed
C3orf1
localization in the inner mitochondrial membrane and showed that mitochondrial viability, membrane potential, and ATPase activity were remarkably reduced upon depletion of
C3orf1
. Microarray data indicated that genes involved in regulation of cell death, migration, and cell-cycle arrest were significantly altered after
C3orf1
depletion for 48 h. The expression of genes involved in focal adhesion, ECM-receptor interaction, and
p53
-signaling pathways were notably altered. Furthermore, cell-cycle arrest genes such as CCNG2 and PTEN as well as genes involved in cell migration inhibition, such as TIMP3 and COL3A1, were upregulated after
C3orf1
depletion in 95D cells. Concurrently, expression of the migration-promoting gene NUPR1 was markedly reduced, as confirmed by real-time PCR. We conclude that
C3orf1
is critical for mitochondrial function, migration, and proliferation in 95D lung carcinoma cells. Depletion of
C3orf1
inhibited cell migration and cell proliferation in association with upregulation of genes involved in cell-cycle arrest and cell migration inhibition. These results suggest that
C3orf1
(TIMMDC1) may be a viable treatment target for lung carcinoma, and that further study of the role of this protein in lung carcinoma pathogenesis is justified.
...
PMID:Depletion of C3orf1/TIMMDC1 inhibits migration and proliferation in 95D lung carcinoma cells. 2539 Oct 42