Background: One of the main malignancies endangering the lives and health of women is cervical cancer. The poor prognosis for cervical cancer is mostly due to metastasis and recurrence. The metastatic spread of cervical cancer cells is largely dependent on the epithelial-mesenchymal transition (EMT) mechanism. Two conclusions have been drawn from earlier research on the function of basic transcription element binding protein 2 (BTEB2) in cervical cancer: there is both tumor promotion and tumor repression. Therefore, the role of BTEB2 in cervical cancer cell metastasis and tumor growth was examined in vitro and in vivo in order to examine the expression of transcription factor BTEB2 in cervical cancer and study its influence on epithelial-mesenchymal transition (EMT) of cervical cancer cells. Methods: Following the collection of samples from 30 cervical cancer patients as well as nearby tissues, BTEB2 expression in cancer tissues was discovered. The acquisition of both cervical cancer cells and healthy cervical cells allowed for the examination of BTEB2 expression in distinct cervical cancer cell lines. Cell lines that showed differential expression were selected and BTEB2 expression was manipulated for grouping. The expression levels of BTEB2 and EMT-associated proteins (E-cadherin, N-cadherin) were assessed, and the viability, proliferation, migration, and invasion of cervical cancer cells were tracked. To create a xenograft tumor model in the mice, BTEB2-regulated cells were obtained and subcutaneously implanted into naked mice. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to find out how much the transcription factor BTEB2 was expressed in the cancer tissues. Lymphocytes that have infiltrated tumors have been identified using hematoxylin-eosin staining. To identify apoptotic cells, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL) was used. Results: The expression of BTEB2 in cervical cancer cells was upregulated (p < 0.05). After interfering with BTEB2, the expression of BTEB2 in cervical cancer cells decreased, cell vitality decreased, and the ability to proliferate, migrate, and invade was weakened (p < 0.05). EMT-related protein detection found that the expression of E-cadherin decreased and the expression of N-cadherin increased (p < 0.05). Nude mouse tumor transplantation experiments found that after interfering with BTEB2, tumor growth was inhibited, the volume decreased, and the expression of BTEB2 in tumor tissues weakened (p < 0.05). Cell apoptosis increased (p < 0.05). Conclusion: The upregulation of transcription factor BTEB2 is involved in the growth and metastasis of cervical cancer. Interfering with BTEB2 leads to a decrease in the vitality of cervical cancer cells, as well as a weakening of their proliferation, migration, and invasion abilities. Tumor growth is suppressed, and this may occur through the inhibition of the EMT process.