Research Paper Volume 13, Issue 2 pp 2379—2396

Dysregulation of FOXD2-AS1 promotes cell proliferation and migration and predicts poor prognosis in oral squamous cell carcinoma: a study based on TCGA data

Knockdown of FOXD2-AS1 decreased OSCC cell proliferation and migration in vitro and in vivo. (A) The relative expression of FOXD2-AS1 in 25 paired tumor and adjacent normal tissues. The expression of FOXD2-AS1 was significantly up-regulated in Tumor tissues. (B) The relative expression of FOXD2-AS1 in 3 OSCC cell lines and Normal oral primary keratinocytes (NOK) cells. (C) Cell nucleus/cytoplasmic fractionation and qRT-PCR showed the subcellular localization of FOXD2-AS1 in Cal27 cells (MALAT1 and β actin were used as separation quality standards and endogenous controls). (D) The relative expression of FOXD2-AS1 after transfected with SiRNA and Smart Silence in Cal27 cell line. (E) The relative expression of PNCK, HOXB8, HOXB9, KRT6C, EPG and DSG1 after FOXD2-AS1 knockdown by SiRNA. (F) FOXD2-AS1 knockdown inhibited the migration capacity of Cal27 cells as detected by wound-healing assay after 48hs. (G) The cell migration abilities of Cal27 cells transfected with SiRNA and Smart silence were determined by transwell assays. (H) The relative mRNA expression of E-cadherin, N-cadherin and Snail in Cal27 cells transfected with SiRNA and Smart silence. (I) The protein expression of E-cadherin, N-cadherin and Snail in Cal27 cells transfected with SiRNA and Smart silence. FOXD2-AS1 knockdown inhibited the proliferation capacity of Cal27 cells as detected by CCK-8 assay (J) and colony formation assay (K). (L) Tumors were collected from different groups after 8 times ASO-FOXD2-AS1/ASO-NC injection. (M) Volume curve of tumors from different groups at the time of injection. (N) Weight of collected tumors from different groups. *p

Figure 7. Knockdown of FOXD2-AS1 decreased OSCC cell proliferation and migration in vitro and in vivo. (A) The relative expression of FOXD2-AS1 in 25 paired tumor and adjacent normal tissues. The expression of FOXD2-AS1 was significantly up-regulated in Tumor tissues. (B) The relative expression of FOXD2-AS1 in 3 OSCC cell lines and Normal oral primary keratinocytes (NOK) cells. (C) Cell nucleus/cytoplasmic fractionation and qRT-PCR showed the subcellular localization of FOXD2-AS1 in Cal27 cells (MALAT1 and β actin were used as separation quality standards and endogenous controls). (D) The relative expression of FOXD2-AS1 after transfected with SiRNA and Smart Silence in Cal27 cell line. (E) The relative expression of PNCK, HOXB8, HOXB9, KRT6C, EPG and DSG1 after FOXD2-AS1 knockdown by SiRNA. (F) FOXD2-AS1 knockdown inhibited the migration capacity of Cal27 cells as detected by wound-healing assay after 48hs. (G) The cell migration abilities of Cal27 cells transfected with SiRNA and Smart silence were determined by transwell assays. (H) The relative mRNA expression of E-cadherin, N-cadherin and Snail in Cal27 cells transfected with SiRNA and Smart silence. (I) The protein expression of E-cadherin, N-cadherin and Snail in Cal27 cells transfected with SiRNA and Smart silence. FOXD2-AS1 knockdown inhibited the proliferation capacity of Cal27 cells as detected by CCK-8 assay (J) and colony formation assay (K). (L) Tumors were collected from different groups after 8 times ASO-FOXD2-AS1/ASO-NC injection. (M) Volume curve of tumors from different groups at the time of injection. (N) Weight of collected tumors from different groups. *p < 0.05, **p < 0.01, ***p < 0.001.