RT Journal Article
SR Electronic
T1 Imipramine Suppresses Tumor Growth and Induces Apoptosis in Oral Squamous Cell Carcinoma: Targeting Multiple Processes and Signaling Pathways
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 3987
OP 3996
DO 10.21873/anticanres.16586
VO 43
IS 9
A1 HSU, LI-CHO
A1 LIN, CHING NI
A1 HSU, FEI-TING
A1 CHEN, YING-TZU
A1 CHANG, PO-LUNG
A1 HSIEH, LING-LING
A1 WANG, HSIAO-YU
A1 LIN, KUANG-HSUAN
A1 HSIAO, HSIN-CHANG
A1 TU, HSI-FENG
YR 2023
UL http://ar.iiarjournals.org/content/43/9/3987.abstract
AB Background/Aim: Oral squamous cell carcinoma (OSCC) has limited treatment options. This study investigated imipramine, a tricyclic antidepressant, as a potential therapy for OSCC using a SAS-bearing xenograft animal model. Materials and Methods: The SAS-bearing xenograft model evaluated imipramine’s impact on tumor growth. The control group received no treatment, while the imipramine-treated group received regular doses. Tumor growth, confirmed by imaging, and histological analysis assessed size and weight. Imipramine’s effects on apoptosis, epithelial-to-mesenchymal transition (EMT), and transcription factors (AKT, ERK, STAT3) were analyzed. Results: Imipramine significantly suppressed tumor growth within 6 days of treatment, with sustained activity. Computer tomography (CT) scans and histology confirmed reduced size and weight by imipramine. Imipramine induced apoptosis via caspase-dependent/-independent pathways, inhibited EMT, and down-regulated phosphorylated AKT, ERK, and STAT3. Conclusion: Imipramine shows promise as an effective OSCC therapy, inhibiting tumor growth, inducing apoptosis, and inhibiting EMT. Its impact on transcription factors and modulation of the AKT/ERK/STAT3 pathway suggest a multifaceted approach.