scholarly journals Suppression of KIF22 Inhibits Cell Proliferation and Xenograft Tumor Growth in Tongue Squamous Cell Carcinoma

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Yi Liu ◽  
Rong-Hua Li ◽  
Gang Ren ◽  
Jin Jiang
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Protein Expression ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Oral Carcinoma ◽  
Xenograft Tumor ◽  
Protein Expression Level ◽  
Xenograft Tumor Growth

Background. Oral carcinoma is the sixth most common cancer and is a serious public health problem, and tongue squamous cell carcinoma (TSCC) is the most common type of oral carcinoma. Kinesin family member 22 (KIF22), also called as kinesin-like DNA binding protein (KID), is a microtubule-based motor protein and binds to both microtubules and chromosomes, transporting organelles, protein, and mRNA. This research aimed at investigating the prognostic significance of KIF22 in TSCC. Patients and Methods. This retrospective research collected 82 paired tissues with TSCC. KIF22 protein expression level was detected by immunohistochemical staining. Suppression of KIF22 with shRNA in CAL-27 and SCC-15 cells was to observe cell proliferation in vitro and xenograft tumor growth in vivo. Results. In TSCC tissues, the protein expression level of KIF22 was increased and correlated with tumor stage, clinical stage, and lymphatic metastasis (P=0.013, P=0.034 and P=0.015, respectively). Suppression of KIF22 inhibited cell proliferation and xenograft tumor growth. Conclusion. KIF22 might play an important role in the progression of TSCC and could serve as a therapeutic target for TSCC.

scholarly journals Knockdown of circ_0011946 targets miR-216a-5p/BCL2L2 axis to regulate proliferation, migration, invasion and apoptosis of oral squamous cell carcinoma cells

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ying Zhou ◽  
Shuhong Zhang ◽  
Zhonghan Min ◽  
Zhongwei Yu ◽  
Huaiwei Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
B Cell Lymphoma ◽  
Luciferase Reporter ◽  
Migration And Invasion

Abstract Background Circular RNAs (circRNAs) are implicated in the development of oral squamous cell carcinoma (OSCC). The aim of current research is to elucidate the role and mechanism of circ_0011946 in the functional behaviors of OSCC cells. Methods Circ_0011946, microRNA (miR)-216a-5p, B cell lymphoma-2-like 2 protein (BCL2L2) abundances were exposed by quantitative reverse transcription polymerase chain reaction (qRT-PCR) or western blot. Cell proliferation, migration, invasion and apoptosis were detected by MTT, colony formation assay, transwell, wound-healing and flow cytometry assays, respectively. Target correlation was tested by dual-luciferase reporter and RNA pull-down assays. An in vivo xenograft experiment was employed to investigate the function of circ_0011946 on tumor growth in vivo. Results Circ_0011946 and BCL2L2 levels were increased, while miR-216a-5p level was decreased in OSCC tissues and cells. Circ_0011946 knockdown impeded proliferation, migration, and invasion, but promoted apoptosis in OSCC cells. Circ_0011946 functioned as a sponge for miR-216a-5p, and BCL2L2 was targeted by miR-216a-5p. Besides, miR-216a-5p or BCL2L2 knockdown partly attenuated the inhibitory influences of circ_0011946 silence or miR-216a-5p overexpression on OSCC cell progression. Furthermore, circ_0011946 post-transcriptionally regulated BCL2L2 through sponging miR-216a-5p. Moreover, circ_0011946 knockdown constrained OSCC tumor growth in vivo. Conclusion Circ_0011946 silence repressed OSCC cell proliferation, migration, and invasion, but promoted apoptosis through the regulation of the miR-216a-5p/BCL2L2 axis.

scholarly journals Exosomal lncRNA ZFAS1 regulates esophageal squamous cell carcinoma cell proliferation, invasion, migration and apoptosis via microRNA-124/STAT3 axis

2019 ◽  
Vol 38 (1) ◽  
Author(s):  
Zhirong Li ◽  
Xuebo Qin ◽  
Wei Bian ◽  
Yishuai Li ◽  
Baoen Shan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Migration And Invasion ◽  
Donor Cells

Abstract Background In recent years, long non-coding RNAs (lncRNAs) are of great importance in development of different types of tumors, while the function of lncRNA ZFAS1 is rarely discussed in esophageal squamous cell carcinoma (ESCC). Therefore, we performed this study to explore the expression of exosomal lncRNA ZFAS1 and its molecular mechanism on ESCC progression. Methods Expression of ZFAS1 and miR-124 in ESCC tissues was detected. LncRNA ZFAS1 was silenced to detect its function in the biological functions of ESCC cells. A stable donor and recipient culture model was established. Eca109 cells transfected with overexpressed and low expressed ZFAS1 plasmid and miR-124 inhibitor labeled by Cy3 were the donor cells, and then co-cultured with recipient cells to observe the transmission of Cy3-ZFAS1 between donor cells and recipient cells. The changes of cell proliferation, apoptosis, invasion, and migration in recipient cells were detected. The in vivo experiment was conducted for verifying the in vitro results. Results LncRNA ZFAS1 was upregulated and miR-124 was down-regulated in ESCC tissues. Silencing of ZFAS1 contributed to suppressed proliferation, migration, invasion and tumor growth in vitro and induced apoptosis of ESCC cells. LncRNA ZFAS1 was considered to be a competing endogenous RNA to regulate miR-124, thereby elevating STAT3 expression. Exosomes shuttled ZFAS1 stimulated proliferation, migration and invasion of ESCC cells and restricted their apoptosis with increased STAT3 and declined miR-124. Furthermore, in vivo experiment suggested that elevated ZFAS1-exo promoted tumor growth in nude mice. Conclusion This study highlights that exosomal ZFAS1 promotes the proliferation, migration and invasion of ESCC cells and inhibits their apoptosis by upregulating STAT3 and downregulating miR-124, thereby resulting in the development of tumorigenesis of ESCC.

scholarly journals EIF3H promotes aggressiveness of esophageal squamous cell carcinoma by modulating Snail stability

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Xiaobin Guo ◽  
Rui Zhu ◽  
Aiping Luo ◽  
Honghong Zhou ◽  
Fang Ding ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Colony Formation ◽  
Tumor Growth And Metastasis

Abstract Background Overexpression of eukaryotic translation initiation factor 3H (EIF3H) predicts cancer progression and poor prognosis, but the mechanism underlying EIF3H as an oncogene remains unclear in esophageal squamous cell carcinoma (ESCC). Methods TCGA database and the immunohistochemistry (IHC) staining of ESCC samples were used and determined the upregulation of EIF3H in ESCC. CCK8 assay, colony formation assay and transwell assay were performed to examine the ability of cell proliferation and mobility in KYSE150 and KYSE510 cell lines with EIF3H overexpression or knockdown. Xenograft and tail-vein lung metastatic mouse models of KYSE150 cells with or without EIF3H knockdown were also used to confirm the function of EIF3H on tumor growth and metastasis in vivo. A potential substrate of EIF3H was screened by co-immunoprecipitation assay (co-IP) combined with mass spectrometry in HEK293T cells. Their interaction and co-localization were confirmed using reciprocal co-IP and immunofluorescence staining assay. The function of EIF3H on Snail ubiquitination and stability was demonstrated by the cycloheximide (CHX) pulse-chase assay and ubiquitination assay. The correlation of EIF3H and Snail in clinical ESCC samples was verified by IHC. Results We found that EIF3H is significantly upregulated in esophageal cancer and ectopic expression of EIF3H in ESCC cell lines promotes cell proliferation, colony formation, migration and invasion. Conversely, genetic inhibition of EIF3H represses ESCC tumor growth and metastasis in vitro and in vivo. Moreover, we identified EIF3H as a novel deubiquitinating enzyme of Snail. We demonstrated that EIF3H interacts with and stabilizes Snail through deubiquitination. Therefore, EIF3H could promote Snail-mediated EMT process in ESCC. In clinical ESCC samples, there is also a positive correlation between EIF3H and Snail expression. Conclusions Our study reveals a critical EIF3H-Snail signaling axis in tumor aggressiveness in ESCC and provides EIF3H as a promising biomarker for ESCC treatment.

scholarly journals RNA m6A demethylase FTO-mediated epigenetic up-regulation of LINC00022 promotes tumorigenesis in esophageal squamous cell carcinoma

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Yuanbo Cui ◽  
Chunyan Zhang ◽  
Shanshan Ma ◽  
Zhe Li ◽  
Wenjie Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epigenetic Modification ◽  
Epigenetic Mechanism ◽  
Potential Biomarker

Abstract Background Long non-coding RNA (LncRNA) controls cell proliferation and plays a significant role in the initiation and progression of esophageal squamous cell carcinoma (ESCC). N6-methyladenosine (m6A) modification now is recognized as a master driver of RNA function to maintain homeostasis in cancer cells. However, how m6A regulates LncRNA function and its role in tumorigenesis of ESCC remain unclear. Methods Multiple ESCC datasets were used to analyze gene expression in tumor tissues and normal tissues. Kaplan-Meier method and the ROC curve were conducted to evaluate the prognostic value and diagnostic value of LINC00022 in ESCC, respectively. Both gain-of-function and loss-of-function experiments were employed to investigate the effects of LINC00022 on ESCC growth in vitro and in vivo. Bioinformatics analysis, colorimetric m6A assay, RIP, MeRIP and co-IP was performed to explore the epigenetic mechanism of LINC00022 up-regulation in ESCC. Results Here we report that m6A demethylation of LncRNA LINC00022 by fat mass and obesity-associated protein (FTO) promotes tumor growth of ESCC in vivo. Clinically, we revealed that LINC00022 was up-regulated in primary ESCC samples and was predictive of poor clinical outcome for ESCC patients. Mechanistically, LINC00022 directly binds to p21 protein and promotes its ubiquitination-mediated degradation, thereby facilitating cell-cycle progression and proliferation. Further, the elevated FTO in ESCC decreased m6A methylation of LINC00022 transcript, leading to the inhibition of LINC00022 decay via the m6A reader YTHDF2. Over-expression of FTO was shown to drive LINC00022-dependent cell proliferation and tumor growth of ESCC. Conclusions Thus, this study demonstrated m6A-mediated epigenetic modification of LncRNA contributes to the tumorigenesis in ESCC and LINC00022, specific target of m6A, serves as a potential biomarker for this malignancy.

Keratin 17 is co-expressed with 14-3-3 sigma in oral carcinoma in situ and squamous cell carcinoma and modulates cell proliferation and size but not cell migration

2015 ◽  
Vol 466 (5) ◽  
pp. 559-569 ◽  
Author(s):  
Toshihiko Mikami ◽  
Satoshi Maruyama ◽  
Tatsuya Abé ◽  
Takanori Kobayashi ◽  
Manabu Yamazaki ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Cell Migration ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Carcinoma In Situ ◽  
Oral Carcinoma ◽  
Keratin 17

scholarly journals Cisplatin Plus Cetuximab Inhibits Cisplatin-Resistant Human Oral Squamous Cell Carcinoma Cell Migration and Proliferation but Does Not Enhance Apoptosis

2021 ◽  
Vol 22 (15) ◽  
pp. 8167
Author(s):  
Hyeong Sim Choi ◽  
Young-Kyun Kim ◽  
Pil-Young Yun
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Cancer ◽  
Oral Squamous Cell Carcinoma ◽  
Protein Expression ◽  
Cell Motility ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cisplatin Resistance ◽  
Resistant Cells

Cisplatin is among the most widely used anticancer drugs used in the treatment of several malignancies, including oral cancer. However, cisplatin treatment often promotes chemical resistance, subsequently causing treatment failure. Several studies have shown that epidermal growth factor receptors (EGFRs) play a variety of roles in cancer progression and overcoming cisplatin resistance. Therefore, this study focused on EGFR inhibitors used in novel targeted therapies as a method to overcome this resistance. We herein aimed to determine whether the combined effects of cisplatin and cetuximab could enhance cisplatin sensitivity by inhibiting the epithelial-to-mesenchymal transition (EMT) process in cisplatin-resistant cells. In vitro analyses of three cisplatin-resistant oral squamous cell carcinoma cells, which included cell proliferation assay, combination index calculation, cell cytotoxicity assay, live/dead cell count assay, Western blot assay, propidium iodide staining assay, scratch assay, and qRT-PCR assay were then conducted. Our results showed that a cisplatin/cetuximab combination treatment inhibited cell proliferation, cell motility, and N-cadherin protein expression but induced E-cadherin and claudin-1 protein expression. Although the combination of cisplatin and cetuximab did not induce apoptosis of cisplatin-resistant cells, it may be useful in treating oral cancer patients with cisplatin resistance given that it controls cell motility and EMT-related proteins.

scholarly journals Metformin Affects Cancer Regulation and Metabolism of Oral Squamous Cell Carcinoma Partially Through Upregulation of H3K27ac 

2020 ◽  
Author(s):  
Shan Liu ◽  
Congyu Shi ◽  
Xiaoru Hou ◽  
Chunjie Li ◽  
Xiangrui Ma ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Tumor Growth ◽  
Histone Modification ◽  
Cell Carcinoma ◽  
Western Blotting ◽  
Squamous Cell ◽  
Underlying Mechanisms

Abstract Objectives Metformin, a first-line drug that has been used for type 2 diabetes treatment, recently attracts broad attention for its therapeutic effects on diverse human cancers. However, its effect and underlying mechanisms in oral squamous cell carcinoma (OSCC) are not well known. Materials and Methods OSCC cells were used to detect the effect of metformin on cell proliferation, colony formation, cell cycle and migration in vitro. Tumor growth of nude mice was conducted to detect the effect of metformin in vivo. Western blotting and immunohistochemistry were used to investigate the effect of metformin on the expression of histone modification in vitro and vivo. The combined effect on cell proliferation and histone modification of metformin and downregulation of EZH2 was detected by CCK8 and western blotting. Additionally, RNA-seq and ChIP-seq was performed to explore the underlying mechanisms of metformin in OSCC.Results Metformin could inhibit OSCC cell proliferation and tumor growth with the increased acetylation at lysine 27 of histone H3 (H3K27ac) in vitro and vivo. The underlying mechanisms were related to cancer regulation and cancer metabolism, affected by the increased H3K27ac. Additionally, metformin could synergize with siRNA-EZH2 to inhibit OSCC cell proliferation independent on the increased H3K27ac.Conclusions Metformin could play anti-cancer role in OSCC progression, with the reprogramming of cancer regulation and metabolism partially regulated by the increased H3K27ac.

miR-204-5p Inhibits Cell Proliferation and Induces Cell Apoptosis in Esophageal Squamous Cell Carcinoma by Regulating Nestin

2021 ◽  
Author(s):  
Beilong Zhong ◽  
Weize Lv ◽  
Huayong Zhang ◽  
Chunxia Lin ◽  
Fei Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Cell Apoptosis ◽  
Tumor Formation ◽  
Xenograft Tumor ◽  
Nestin Expression

Abstract PurposeThis study aimed to investigate the relationship between miR-204-5p and Nestin in esophageal squamous cell carcinoma (ESCC). MethodsThe expression levels of miR-204-5p and Nestin were tested by quantitative real-time polymerase chain reaction (q-PCR) and Western blotting, respectively. The colony formation assay was used to assess cell proliferation. The flow cytometry and TUNEL assay were used to examine cell apoptosis. Tumorigenesis was evaluated using a murine xenograft tumor model. ResultsESCC tissues and cell lines exhibited decreased miR-204-5p expression and increased Nestin expression, while the opposite results were found in paired para-carcinoma tissues and esophageal epithelial cell lines. The Luciferase reported assay confirmed that Nestin was the direct target of miR-204-5p. In vitro, miR-204-5p inhibited cell proliferation and induced apoptosis through regulating Nestin expression. In vivo, miR-204-5p inhibited xenograft tumor formation. ConclusionIn conclusion, these results indicate that miR-204-5p inhibits cell proliferation and induces cell apoptosis in ESCC through regulating Nestin.

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