Human Tongue Squamous Cell Carcinoma Research Articles

MiR-26b is downregulated in human tongue squamous cell carcinoma and regulates cell proliferation and metastasis through a COX-2-dependent mechanism.

MicroRNAs (miRNAs) are important gene regulators that play a profound role in tumorigenesis. Previous studies have revealed that miR-26b is downregulated in a wide range of malignant tumors and plays an important role in the regulation of carcinogenesis and tumor progression. In the present study, we revealed that miR-26b expression was decreased in human tongue squamous cell carcinoma and was associated with clinical stage, lymph node metastasis and survival prognosis. Ectopic expression of miR-26b suppressed the proliferation and metastasis of human tongue squamous cell carcinoma cells. Using a luciferase reporter assay, combined with western blot analysis results, we identified PTGS2 (prostaglandin-endoperoxide synthase-2, encoding COX-2) as the functional target of miR-26b. Specific inhibition of COX-2 activity by nimesulide further confirmed that miR-26b was able to regulate the cell proliferation and metastasis of the human tongue squamous cell carcinoma cells through a COX-2-dependent mechanism. Taken together, these results suggest that miR-26b serves as a tumor suppressor by targeting COX-2 and calls for the use of miR-26b as a potential therapeutic tool for human tongue squamous cell carcinoma, where COX-2 is often hyperactivated.

Patterns of cancer cell sphere formation in primary cultures of human oral tongue squamous cell carcinoma and neck nodes.

Recently a sub-population of cells with stem cell characteristics, reported to be associated with initiation, growth, spread and recurrence, has been identified in several solid tumors including oral tongue squamous cell carcinoma (OTSCC). The aim of our pilot study was to isolate CD44+ cancer stem cells from primary cultures of OTSCC and neck node Level I (node-I) biopsies, grow cell spheres and observe their characteristics in primary cultures. Parallel cultures of hyperplastic lesions of tongue (non-cancer) were set up as a control. Immunohistochemistry was used to detect CD44/CD24 expression and magnetic activated cell sorting to isolate CD44+ cell populations followed by primary cell culturing. Both OTSCC and node-I biopsies produced floating spheres in suspension, however those grown in hyperplastic and node-I primary cultures did not exhibit self-renewal properties. Lymph node metastatic OTSCC, express higher CD44/CD24 levels, produce cancer cell spheres in larger number and rapidly (24 hours) compared to node negative OTSCC (1 week) and non-cancer specimens (3 weeks). In addition, metastatic OTSCC have the capacity for proliferation for up to three generations in primary culture. This in vitro system will be used to study cancer stem cell behavior, therapeutic drug screening and optimization of radiation dose for elimination of resistant cancer cells.Electronic supplementary materialThe online version of this article (doi:10.1186/s12935-014-0143-3) contains supplementary material, which is available to authorized users.

Subcellular location and photodynamic therapeutic effect of chlorin e6 in the human tongue squamous cell cancer Tca8113 cell line

The present study aimed to investigate the distribution and photodynamic therapeutic effect of chlorin e6 (Ce6) in the human tongue squamous cell carcinoma Tca8113 cell line in vitro. The distribution of Ce6 in the Tca8113 cells was observed in situ combined with mitochondrial and lysosomal fluorescent probes. Next, 630-nm semiconductor laser irradiation was performed. The MTS colorimetric method was used to determine cell survival. Annexin V fluorescein isothiocyanate/propidium iodide (PI) double staining was used to detect early apoptosis following photodynamic therapy (PDT). The flow cytometer was used to analyze the DNA content subsequent to PI-staining. It was observed that Ce6 could combine with the cellular membrane following 30 min of incubation with the Tca8113 cells. As the length of incubation increased, Ce6 gradually entered the cells in a particular distribution and reached saturation by 3 h. Co-localization analysis demonstrated that Ce6 was more likely to be present in the mitochondria than in the lysosomes. The cells incubated with 5 μg/ml Ce6 for 24 h exhibited a low toxicity of 5%, however, following light irradiation, Ce6-PDT was able to kill the Tca8113 cells in vitro. The cell toxicity was positively correlated with Ce6 concentration and light dose, therefore, the effect of Ce6 was concentration/dose-dependent (P<0.01). The lower Ce6 concentrations and light doses could significantly induce apoptosis in the Tca8113 cells, while higher doses increased necrosis/percentage of dead cells. In summary, Ce6 saturated the Tca8113 cells following 3 h of incubation. Furthermore, Ce6-PDT effectively killed the cultured Tca8113 cells in vitro at a safe concentration. At a low concentration and light dose, Ce6 is more likely to induce cell apoptosis via the mitochondria than the lysosomes.

Alisertib (MLN8237), a selective Aurora-A kinase inhibitor, induces apoptosis in human tongue squamous cell carcinoma cell both in vitro and in vivo.

Aurora-A kinases are overexpressed in many cancer tissues and cells. Alisertib is an investigational, orally administered, selective, small-molecule Aurora-A kinase inhibitor with preclinical activity against a broad range of tumors. Our study was aimed to detect the effects of alisertib on human tongue squamous cell carcinoma (HTSCC). Treatment of a human tongue squamous cell carcinoma cell line, HSC-3, with alisertib to inhibition of Aurora-A kinases reduced proliferation and induced apoptosis, which was accompanied by activation of the ATM/Chk2/p53 pathway. In vivo, inhibition of Aurora-A kinases in established xenografted tumors decreased tumor size and weight. Kaplan-Meyer survival analysis demonstrated that the cumulative survival time of mice without Aurora-A kinases was significantly longer than those with Aurora-A kinases. Our data provide the basis for developing alisertib to treat human tongue squamous cell carcinoma.

Overexpression of ZFX and its involvement in squamous cell carcinoma of the tongue.

Zinc finger protein, X-linked (ZFX) has been identified as a transcriptional factor and is implicated in the development of variant types of cancer. Furthermore, it has been reported that ZFX is essential for the survival and self-renewal of embryonic stem cells. To investigate the involvement of ZFX in squamous cell carcinoma of the tongue, in the present study, we explored the expression of ZFX in clinical specimens from patients with squamous cell carcinoma of the tongue and the correlation between ZFX expression and multiple clinical pathological parameters. We further evaluated the impact of ZFX knockdown on the proliferation, colony formation ability, cell cycle distribution and survival of two human tongue squamous cell carcinoma cell lines to explore its critical role in the development of squamous cell carcinoma of the tongue. Our results showed that ZFX expression was aberrantly higher in samples from patients with squamous cell carcinoma of the tongue and revealed that ZFX expression is positively correlated with tumor grade and stage. Consistent with these findings, we further found that ZFX knockdown impaired cell proliferation and colony formation ability and induced cell apoptosis and cell cycle arrest in two human tongue squamous cell carcinoma cell lines. Our results indicate that ZFX is essential for the development and progression of squamous cell carcinoma of the tongue and represents a potential target for the development of effective therapy.

Effect of A disintegrin and metalloproteinase 10 gene silencing on the proliferation, invasion and migration of the human tongue squamous cell carcinoma cell line TCA8113.

The present study aimed to investigate the effect of A disintegrin and metalloproteinase 10 (ADAM10) gene silencing on the proliferation, migration and invasion of the human tongue squamous cell carcinoma cell line TCA8113. RNA interference was used to knock down the expression of ADAM10 in the TCA8113 cell line and the proliferation, migration and invasive ability of the treated cells were observed in vitro. The expression levels of epidermal growth factor receptor (EGFR) and E-cadherin in the treated cells were determined by western blot analysis. The proliferation, migration and invasion abilities of cells in the ADAM10 siRNA-treated group were significantly lower than those in the control groups (P<0.05). In addition, compared with the control groups, the expression levels of EGFR and E-cadherin in the ADAM10 siRNA-treated cells were significantly decreased (P<0.05) and increased (P<0.05), respectively. These results suggested that ADAM10 is important in regulating the proliferation, invasion and migration of the human tongue squamous cell carcinoma cell line TCA8113 and that the mechanism may, at least in part, be associated with the upregulation of EGFR and the downregulation of E-cadherin.

Apoptotic Effect of Co-treatment with Curcumin and Cisplatin on SCC25 Human Tongue Squamous Cell Carcinoma Cell Line

Apoptotic Effect of Co-treatment with Curcumin and Cisplatin on SCC25 Human Tongue Squamous Cell Carcinoma Cell Line

Sphingosine kinase 1 mediates head & neck squamous cell carcinoma invasion through sphingosine 1-phosphate receptor 1.

BackgroundHead and neck squamous cell carcinoma (HNSCC) is characterized by aggressive loco-regional invasion. Sphingosine kinase1 (SphK1), an enzyme in sphingolipid metabolism, is emerging as a key player in HNSCC pathology. The observation that SphK1 is overexpressed in all HNSCC stages and is associated with depth of tumor invasion, metastasis and clinical failure underscores the importance of SphK1 in HNSCC pathology. Still, the mechanisms underlying SphK1 regulation of invasion have not been delineated. Therefore, we sought to mechanistically describe how SphK1 regulates invasion in HNSCC.MethodsInvasion assays were used to measure invasive ability of SphK1 overexpressing human tongue squamous cell carcinoma (SCC-25 cells). Western blotting, quantitative qPCR, ELISA and zymography were used to measure the effect of SphK1 and sphingosine 1-phoshate receptor 1 (S1P1) on invasion measures, MMP-2/9, E-cadherin, EGFR, IL-6/STAT3, in SCC-25 cells.ResultsSphK1 expression is elevated in cells with an invasive phenotype as compared to non-invasive phenotype. We show SphK1 overexpression increased EGF-induced EGFR/ERK and AKT activity, increased matrix metalloproteinase (MMP)-2/9 mRNA and reduced E-cadherin. SphK1 overexpression also increased IL-6 concentration and EGF-induced STAT3 phosphorylation, exemplifying that SphK1 modulates IL-6/STAT3 signaling. Notably, we show that S1P1 knockdown reduced IL-6/STAT3 signaling, representing another pathway by which SphK1/S1P regulates invasion.ConclusionsTaken together, our data suggest that SphK1 sits at the hub of multiple key signaling cascades, all which have been implicated in the regulation of invasiveness, making SphK1 an attractive target for the development of HNSCC therapies.

Comparison of ultracentrifugation and density gradient separation methods for isolating Tca8113 human tongue cancer cell line-derived exosomes.

The aim of the present study was to compare the method of ultracentrifugation and density gradient separation for isolating Tca8113 human tongue squamous cell carcinoma cell line-derived exosomes. The exosomes were obtained from the culture supernatant of cultured Tca8113 cells, respectively, followed by identification with transmission electron microscopy observation and western blot analysis. The two different methods were then compared by the morphology, the distribution range of the particle size and the concentration of proteins of the extracted exosomes. In vitro, Tca8113 cells can secrete a large amount of vesicle-like structures, which are identified as exosomes by the presence of the surface markers, Hsp-70 and Alix. The protein profile of the two products are almost the same, however the particle size distribution of the exosomes extracted with density gradient centrifugation are more limited, between 40–120 nm, and these have a higher protein concentration. The results indicate that Tca8113 cells can secrete exosomes in vitro, and the density gradient separation methods for purifying exosomes is improved, which is helpful for future research and application of exosomes.

Hyperthermia inhibited the migration of tongue squamous cell carcinoma through TWIST2.

Hyperthermia has been shown promising in the treatment of head and neck squamous cell carcinoma (HNSCC); however, the mechanism underlying hyperthermia reducing tumor metastasis is poorly elucidated. TWIST2, an important transcription factor of epithelial-mesenchymal transition (EMT), plays a critical role in the tumor progression and metastasis. The role of TWIST2 in tongue squamous cell carcinoma (TSCC) and its association with hyperthermia still have not been reported. The correlations between TWIST2 expression and the clinical-pathologic characteristics of 89 patients with TSCC were evaluated by immunohistochemical staining. TSCC cell lines transfected with siRNA against TWIST2 were heated for 40 min at 42.5°C, and the migration capability of cells was examined by migration assay. Xenograft tumors in nude mice were treated by hyperthermia, and TWIST2 expression was measured. Our data showed that TWIST2 expression was associated with the metastasis of human TSCC. In Tca8113 and Cal-27 cells, TWIST2-siRNA treatment can reduce cell migration ability and has no effect on the cell proliferation and apoptosis. Hyperthermia can decrease the level of TWIST2 in TSCC and inhibit the migration of cells. This demonstrated that hyperthermia might decrease the migration of Tca8113 and Cal-27 cells by reducing TWIST2 expression. Altogether, these findings suggest an as yet undescribed link between TWIST2 and hyperthermia in TSCC.

Apoptosis of human tongue squamous cell carcinoma cell (CAL-27) induced by Lactobacillus sp. A-2 metabolites.

ObjectiveTo study the effect of Lactobacillus sp. A-2 metabolites on viability of CAL-27 cells and apoptosis in CAL-27 cells.MethodsLactobacillus sp. A-2 metabolites 1 and 2 (LM1 and LM2) were obtained by culturing Lactobacillus sp. A-2 in reconstituted whey medium and whey-inulin medium; the cultured CAL-27 cells were treated with different concentrations of LM1 and LM2 (0, 3, 6, 12, 24, 48 mg/mL) and assayed by methyl thiazolyltetrazolium (MTT) method; morphological changes of apoptotic cell were observed under fluorescence microscopy by acridine orange (Ao) fluorescent staining; flow cytometry method (FCM) and agarose gel electrophoresis were used to detect the apoptosis of CAL-27 cells treated LM1 and LM2.ResultsThe different concentrations of LM1 and LM2 could restrain the growth of CAL-27 cells, and in a dose-dependent manner; the apoptosis of CAL-27 cells was obviously induced and was time-dependent. ConclusionsViability of CAL-27 cells was inhibited by Lactobacillus sp. A-2 metabolites; Lactobacillus sp. A-2 metabolites could induce CAL-27 cells apoptosis; study on the bioactive compounds in the Lactobacillus sp. A-2 metabolites and their molecular mechanism is in progress.

Altered Histone Mark Deposition and DNA Methylation at Homeobox Genes in Human Oral Squamous Cell Carcinoma

We recently reported a role of polycomb repressive complex 2 (PRC2) and PRC2 trimethylation of histone 3 lysine 27 (H3K27me3) in the regulation of homeobox (HOX) (Marcinkiewicz and Gudas, 2013, Exp Cell Res) gene transcript levels in human oral keratinocytes (OKF6-TERT1R) and tongue squamous cell carcinoma (SCC) cells. Here, we assessed both the levels of various histone modifications at a subset of homeobox genes and genome wide DNA methylation patterns in OKF6-TERT1R and SCC-9 cells by using ERRBS (enhanced reduced representation bisulfite sequencing). We detected the H3K9me3 mark at HOXB7, HOXC10, HOXC13, and HOXD8 at levels higher in OKF6-TERT1R than in SCC-9 cells; at IRX1 and SIX2 the H3K9me3 levels were conversely higher in SCC-9 than in OKF6-TERT1R. The H3K79me3 mark was detectable only at IRX1 in OKF6-TERT1R and at IRX4 in SCC-9 cells. The levels of H3K4me3 and H3K36me3 marks correlate with the transcript levels of the assessed homeobox genes in both OKF6-TERT1R and SCC-9. We detected generally lower CpG methylation levels on DNA in SCC-9 cells at annotated genomic regions which were differentially methylated between OKF6-TERT1R and SCC-9 cells; however, some genomic regions, including the HOX gene clusters, showed DNA methylation at higher levels in SCC-9 than OKF6-TERT1R. Thus, both altered histone modification patterns and changes in DNA methylation are associated with dysregulation of homeobox gene expression in human oral cavity SCC cells, and this dysregulation potentially plays a role in the neoplastic phenotype of oral keratinocytes.

Expression, regulation and roles of miR‐26a and MEG3 in tongue squamous cell carcinoma

MicroRNA miR-26a and long noncoding RNA (lncRNA) MEG3 gene have been independently reported to be tumor suppressor genes in various cancers, but neither has been previously associated with tongue squamous cell carcinoma (TSCC). We report here that miR-26a and lncRNA MEG3 gene expression were both strongly reduced in TSCC compared with levels in matched nonmalignant tissues, and combined low expression levels of both miR-26a and MEG3 emerged as an independent prognostic factor for poor clinical outcome in TSCC patients. Assays in the human TSCC cell lines SCC-15 and CAL27 showed that miR-26a targets the DNA methyltransferase 3B transcript and that its inhibition may result in the upregulation of MEG3, providing a plausible link between the observed reduction of miR-26a and MEG3 in TSCC tissue. Furthermore, the overexpression of miR-26a or MEG3 in SCC-15 and CAL27 cells inhibited cell proliferation and cell cycle progression, and promoted cell apoptosis. Considering the poor prognostic outcomes associated with reduced miR-26a and MEG3, our findings imply that these factors likely play important antitumor effects in TSCC pathogenesis. Furthermore, they represent potential prognostic biomarkers for stratification of TSCC patients.

Signal transducer and activator of transcription-3 inhibitor WP1066 affects human tongue squamous cell carcinoma proliferation and apoptosis in vitro and in vivo

To investigate the antitumour molecular mechanisms of WP1066 (STAT-3 inhibitor ) to human tongue squamous cell carcinoma in vitro and in vivo. WP1066 was used to inhibit the p-STAT-3 expression in Tscca human tongue squamous cell carcinoma cell line .Real-time PCR was used to detect the microRNA-21 expression after treatment with DMSO and WP1066. Methyl thiazolyl tatrozolium (MTT) assay was employed to determine cell survival. Flow cytometry (FCM) was used to measure apoptosis. The expression level of STAT-3/p-STAT-3, programmed cell death protein 4 (PDCD-4), antigen 67 (Ki-67), B cell lymphoma 2 (Bcl-2) and cleaved cysteinyl aspartate specific proteinase-3 (CCASP-3) was examined by Western blotting. Luciferase reporter gene assay was conducted to verify the regulation of STAT-3 to microRNA-21. Tscca xenograft tumor model was established in BALB/c nude mice and the tumors were divided into control, DMSO and WP1066 treated groups. The tumor tissues were measured by immunohistochemistry stain and terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) assay. STAT-3/p-STAT-3 protein was suppressed after treatment with WP1066 (STAT-3:F = 15.336, P = 0.004, p-STAT-3: F = 52.837, P = 0.000). MicroRNA-21 relative expression level was down-regulated (F = 8.197, P = 0.019). Cell survival rate was significantly reduced after treatment with WP1066 than control groups (F = 94.388, P = 0.000). Early apoptosis rate increased after treatment with WP1066 (F = 217.080, P = 0.000) . PDCD-4 and cleaved cysteinyl aspartate specific proteinase-3 (CCASP-3) protein expression was increased after treatment with WP1066 (PDCD-4:F = 8.771, P = 0.017; CCASP-3: F = 26.611, P = 0.001) .Ki-67 and Bcl-2 protein was down regulated (Ki-67:F = 5.854, P = 0.039; Bcl-2:F = 125.502, P = 0.000). Luciferase reporter gene assay proved that STAT-3 combined with specific promoter region of microRNA-21.In vivo, the tumor volume after treatment with WP1066 was significantly smaller than control groups by the end of observation (F = 15.390, P = 0.000) .Immunological histological chemistry indicated that PDCD-4 and CCASP-3 protein expression was up-regulated simultaneously while Ki-67 and Bcl-2 protein of tumor tissue was down-regulated after treatment with WP1066 than control groups. TUNEL assay suggested that apoptosis index rose after treatment with WP1066 than control groups (F = 133.368, P = 0.000) . WP1066 affected Tscca cancer cell proliferation and apoptosis via inhibiting STAT-3/microRNA-21.WP1066 provided new direction and possibility to human tongue squamous cell carcinoma therapy.

Antimutagenic and antioxidative activities of sandy tea and its in vitro anticancer effect on TCA8113 human tongue squamous carcinoma cells (647.7)

Sandy tea is a traditional and popular drink in China. The aim of this study was to determine the antioxidant activity, antimutagenic activity of sandy tea and its in vitro anticancer effect on TCA8113 human tongue squamous carcinoma cells. The antioxidant effects were determined by measuring the 1,1‐diphenyl‐2‐picryhydrazyl (DPPH) free radical舉 and hydroxyl radical舉scavenging activity. The sandy tea extract demonstrated high antioxidant activity in the assays of DPPH and hydroxyl radical舉scavenging activity. At concentrations of 1.25 and 2.5 mg/plate, sandy tea exhibited anti‐mutagenicity with N‐methyl‐N'‐nitro‐N‐nitrosoguanidine (MNNG) in the Salmonella typhimurium TA100 strain. MTT assay and RT‐PCR assay were employed to check the anticancer effects on TCA8113 cancer cells. At the concentration of 200 µg/ml, sandy tea (81%) showed the best inhibitory effect on TCA8113 human tongue squamous carcinoma cells compared to the other concentrations. Compared with 100 µg/ml and 50 µg/ml of sandy tea extracts, 200 µg/ml of sandy tea induced apoptosis, up‐regulated mRNA expressions of Bax, caspase‐3 and caspase‐9, and down‐regulated Bcl‐2 expression. These results suggest that sandy tea possesses good antioxidant activity and anticancer effect on TCA8113 human tongue squamous carcinoma cells.

Altered intracellular trafficking of EGFR by extracellular glucose concentration in squamous carcinoma cells (948.2)

Cancer cells usually exhibit the increased uptake of glucose than normal cells via glucose transporters, and pathogenesis and progression of squamous cell carcinoma are closely related to the expression of epidermal growth factor receptor (EGFR). To connect these two events, we here examined whether intracellular translocation of EGFR is regulated by glucose concentration. Human gingival, tongue and skin squamous carcinoma cells (HSC‐2, HSC‐3 and A431) were grown in D‐MEM in the presence of either high or low concentration of glucose (25mM or 5.5mM: HG or LG). When cancer cells were maintained in HG medium, the expression of EGFR with a molecular size of 170kDa was observed as assessed by Western blot analysis. In contrast, cells cultured in LG medium showed the major positive band to anti‐EGFR antibody, with 140kDa. We assumed the size difference is caused by glycosylation, as the treatment of cell extract with 170kDa band by N‐glycosidase produced the band with 140kDa. We further examined the effect of tunicamycin (10μM) to inhibit glycosylation process, resulting in that EGFR turned into 140kDa even if cells were cultured in HG medium. Biotinylation assay revealed that the only 170kDa protein was detected, indicating that the 170kDa bands are present at the plasma membrane. These results suggest that glucose concentration regulates glycosylation of EGFR and subsequent translocation to the plasma membrane.

Mechanism Underlying Curcumin-induced Apoptosis and Cell Cycle Arrest on SCC25 Human Tongue Squamous Cell Carcinoma Cell Line

Mechanism Underlying Curcumin-induced Apoptosis and Cell Cycle Arrest on SCC25 Human Tongue Squamous Cell Carcinoma Cell Line

A role for cancer‐associated fibroblasts in inducing the epithelial‐to‐mesenchymal transition in human tongue squamous cell carcinoma

Lymph node metastasis is a prominent clinical feature of tongue squamous cell carcinoma (TSCC) and is associated with a higher mortality rate. Carcinoma-associated fibroblasts (CAFs), a major component of the tumor microenvironment (TME), play an important role in tumor progression, and are associated with a poor prognosis. The aim of this study was to examine the role of CAFs in promoting the invasion of TSCC through the epithelial-to-mesenchymal transition (EMT). A series of matched CAF and normal fibroblast (NF) pairs were assessed for cell morphology and for the expression of alpha smooth muscle actin (α-SMA), stromal cell-derived factor-1 (SDF1), fibroblast-activating protein (FAP), vimentin, and cytokeratin (CK) markers. Transwell assays, Western blot analysis, reverse transcription-PCR, and immunofluorescence staining were used to assess the role of CAFs, as compared to that of NFs, in promoting proliferation, migration, invasion, and EMT in TSCC. Both CAF and NF primary cultures expressed vimentin but not CK. CAFs showed significantly higher α-SMA protein levels, SDF1 secretion, and mRNA levels of α-SMA, SDF1, and FAP. We also found that co-culture with CAFs enhanced the proliferation and invasion of SCC9 cells. Moreover, co-culture with CAFs induced upregulation of the EMT markers fibronectin and vimentin, downregulation of E-cadherin, and enhanced invasion in SCC9 cells. These results suggest that CAFs induce EMT marker expression and functional changes in TSCCs.

English

English

RECQL1 Plays an Important Role in the Development of Tongue Squamous Cell Carcinoma

Background/Aims: RECQL1, a member of the human RECQ helicase family, participates in DNA repair. Recent reports showed that RECQL1 silencing in cancer cells resulted in mitotic catastrophe, which prevented tumor growth in murine models. However, its therapeutic potential has never been examined in tongue squamous cell carcinoma (SCC). Methods: To explore the role of RECQL1 in the development of tongue SCC, we used RNA interference technology to silence RECQL1 in SCC-9 and SCC-15 human tongue SCC cell lines, and to subsequently evaluate its effects both in vitro and in vivo. Results: After RECQL1 was silenced in SCC cells by siRNA, we observed downregulation of RECQL1 mRNA and protein in cancer cells. RECQL1 is one of the predicted miR-203 targets, and we found that miR-203 downregulated the expression of RECQL1 at the post-transcriptional level. RECQL1-shRNA or miR-203 overexpression inhibited SCC-9 cell growth. In addition, there was accumulation of cells in the sub-G1 fraction and increased apoptosis 72 h post-transfection. In addition, knockdown of RECQL1 led to a strong anticancer effect, as the tumorigenicity of SCC-9 cells was inhibited in vivo. Moreover, we found that two immunosuppressive factors were also significantly downregulated upon RECQL1 knockdown or miR-203 overexpression in vitro. Conclusion: Collectively, these results indicate that RECQL1 plays an important regulatory role in cancer cell proliferation and tumor progression.