PT - JOURNAL ARTICLE AU - HSU, LI-CHO AU - LIN, CHING NI AU - HSU, FEI-TING AU - CHEN, YING-TZU AU - CHANG, PO-LUNG AU - HSIEH, LING-LING AU - WANG, HSIAO-YU AU - LIN, KUANG-HSUAN AU - HSIAO, HSIN-CHANG AU - TU, HSI-FENG TI - Imipramine Suppresses Tumor Growth and Induces Apoptosis in Oral Squamous Cell Carcinoma: Targeting Multiple Processes and Signaling Pathways AID - 10.21873/anticanres.16586 DP - 2023 Sep 01 TA - Anticancer Research PG - 3987--3996 VI - 43 IP - 9 4099 - http://ar.iiarjournals.org/content/43/9/3987.short 4100 - http://ar.iiarjournals.org/content/43/9/3987.full SO - Anticancer Res2023 Sep 01; 43 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.