Sonic Hedgehog–GLI Family Zinc Finger 1 Signaling Pathway Promotes the Growth and Migration of Pancreatic Cancer Cells by Regulating the Transcription of Eukaryotic Translation Initiation Factor 5A2

Nowadays, pancreatic cancer has been recognized as one of the most fatal malignancies worldwide, the molecular mechanism of which is still not fully understood. In this study, we aimed to uncover the fundamental functions of the eukaryotic translation initiation factor 3H subunit (EIF3H) in the development and progression of pancreatic cancer. Firstly, the results of immunohistochemical (IHC) staining revealed that EIF3H was highly expressed in pancreatic cancer. Moreover, lentiviruses were used to deliver shRNAs into pancreatic cancer cells for silencing EIF3H. Furthermore, the loss-of-function assays demonstrated that knockdown of EIF3H could inhibit the progression of pancreatic cancer cells by reducing proliferation capacity, promoting apoptosis, arresting cell cycle in G2 and suppressing cell migration. In summary, EIF3H may play a critical role in the development and progression of pancreatic cancer, which possesses the potential to act as a therapeutic target for pancreatic cancer treatment.

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Antisense oligonucleotide targeting eukaryotic translation initiation factor 4E reduces growth and enhances chemosensitivity of non-small-cell lung cancer cells

Cancer Gene Therapy ◽

10.1038/cgt.2015.34 ◽

2015 ◽

Vol 22 (8) ◽

pp. 396-401 ◽

Cited By ~ 17

Author(s):

S C Thumma ◽

B A Jacobson ◽

M R Patel ◽

B W Konicek ◽

M J Franklin ◽

...

Keyword(s):

Lung Cancer ◽

Cancer Cells ◽

Translation Initiation ◽

Antisense Oligonucleotide ◽

Small Cell ◽

Translation Initiation Factor ◽

Initiation Factor ◽

Small Cell Lung ◽

Eukaryotic Translation ◽

Eukaryotic Translation Initiation

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N1-Guanyl-1,7-Diaminoheptane Sensitizes Estrogen Receptor Negative Breast Cancer Cells to Doxorubicin by Preventing Epithelial-Mesenchymal Transition through Inhibition of Eukaryotic Translation Initiation Factor 5A2 Activation

Cellular Physiology and Biochemistry ◽

10.1159/000430209 ◽

2015 ◽

Vol 36 (6) ◽

pp. 2494-2503 ◽

Cited By ~ 11

Author(s):

Yu Liu ◽

Rongrong Liu ◽

Peifen Fu ◽

Feiya Du ◽

Yun Hong ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Translation Initiation ◽

Breast Cancer Cells ◽

Epithelial Mesenchymal Transition ◽

Translation Initiation Factor ◽

Initiation Factor ◽

Mesenchymal Transition ◽

Eukaryotic Translation ◽

Eukaryotic Translation Initiation

Background: Approximately 30% of breast cancer does not express the estrogen receptor (ER), which is necessary for endocrine-based therapy approaches. Many studies demonstrated that eukaryotic translation initiation factor 5A2 (eIF5A2) serves as a proliferation-related oncogene in tumorigenic processes. Methods: The present study used cell viability assays, EdU incorporation assays, western blot, and immunofluorescence to explore whether N1-guanyl-1,7-diaminoheptane (GC7), which inhibits eIF5A2 activation, exerts synergistic cytotoxicity with doxorubicin in breast cancer. Results: We found that GC7 enhanced doxorubicin cytotoxicity in ER-negative HCC1937 cells but had little effect in ER-positive MCF-7 and Bcap-37 cells. Administration of GC7 reversed the doxorubicin-induced epithelial-mesenchymal transition (EMT) in ER-negative breast cancer cells. Knockdown of eIF5A2 by siRNA inhibited the doxorubicin-induced EMT in ER-negative HCC1937 cells. Conclusion: These data demonstrated that GC7 combination therapy may enhance the therapeutic efficacy of doxorubicin in estrogen negative breast cancer cells by preventing EMT through inhibition of eIF5A2 activation.

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