@article {AKANDA3349, author = {MD RASHEDUNNABI AKANDA and JEE SOO PARK and MYUNG-GIUN NOH and GEUN-HYOUNG HA and YOUNG SOOK PARK and JAE-HYUK LEE and KYUNG-SUB MOON and CHUNG KWON KIM and KYUNG-HWA LEE}, title = {TACC3 Promotes Gastric Carcinogenesis by Promoting Epithelial-mesenchymal Transition Through the ERK/Akt/cyclin D1 Signaling Pathway}, volume = {41}, number = {7}, pages = {3349--3361}, year = {2021}, doi = {10.21873/anticanres.15123}, publisher = {International Institute of Anticancer Research}, abstract = {Background/Aim: The present study investigated the oncogenic functions of TACC3 in the progression of gastric cancer (GC). Materials and Methods: We analysed TACC3 in relation to cell growth, invasion capability, expression of epithelial-mesenchymal transition (EMT)-related markers, and ERK/Akt/cyclin D1 signaling factors. The correlation between the immunohistochemically confirmed expression of TACC3 and clinical factors was also analyzed. Results: The increased proliferation and invasion of TACC3-over-expressing GC cells was accompanied by altered regulation of EMT-associated markers and activation of ERK/Akt/cyclin D1 signaling. Immunohistochemical analysis of TACC3 in human GC tissues revealed that its expression is correlated with aggressive characteristics and poor prognosis of intestinal-type GC. Conclusion: TACC3 contributes to gastric tumorigenesis by promoting EMT via the ERK/Akt/cyclin D1 signaling pathway. The correlation between TACC3 expression and multiple clinicopathological variables implies that its effective therapeutic targeting in GC will depend on the tumor subtype.}, issn = {0250-7005}, URL = {https://ar.iiarjournals.org/content/41/7/3349}, eprint = {https://ar.iiarjournals.org/content/41/7/3349.full.pdf}, journal = {Anticancer Research} }