LncRNA XIST promotes the progression of laryngeal squamous cell carcinoma via sponging miR-125b-5p to modulate TRIB2

Abstract Objective: X inactivate-specific transcript (XIST) is an attractive long noncoding RNA (lncRNA) functioning as an indicator of various human tumors, including laryngeal squamous cell carcinoma (LSCC). The present study was conducted to explore a novel regulatory network of lncRNA XIST in LSCC cells. Materials and methods: Quantitative real-time polymerase chain reaction (QRT-PCR) was used to detect the expression levels of XIST, miR-125b-5p and TRIB2 in LSCC cells and tissues. Cell proliferation, apoptosis, migration and invasion were detected by Cell Counting Kit-8 (CCK-8), flow cytometry and Transwell assays, separately. The relationship among XIST, miR-125b-5p and tribbles homolog 2 (TRIB2) was predicted by starBase v2.0 or TargetScan and confirmed by Dual-luciferase reporter assay. The TRIB2 protein expression was quantified by Western blot assay. Murine xenograft model was utilized to validate the role of XIST in vivo. Results: XIST was notably up-regulated in LSCC tissues and cells, and the high level of XIST was associated with the low survival rate of LSCC patients. XIST knockdown markedly repressed cell proliferation, migration and invasion and promoted the apoptosis of LSCC cells and the effects were antagonized by loss of miR-125b-5p. MiR-125b-5p was a target of XIST in LSCC cells, and it could bind to TRIB2 as well. Moreover, XIST-loss-induced down-regulation of TRIB2 could be significantly reversed by miR-125b-5p knockdown. XIST promoted the growth of LSCC tumor in vivo. Conclusion: LncRNA XIST promoted the malignance of LSCC cells partly through competitively binding to miR-125b-5p, which in turn increased TRIB2 expression.

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Circular RNA circ_0006168 enhances Taxol resistance in esophageal squamous cell carcinoma by regulating miR-194-5p/JMJD1C axis

Cancer Cell International ◽

10.1186/s12935-021-01984-y ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Fanyong Qu ◽

Lina Wang ◽

Caiyan Wang ◽

Lingxia Yu ◽

Kaikai Zhao ◽

...

Keyword(s):

Cell Proliferation ◽

Squamous Cell Carcinoma ◽

Esophageal Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Cell Counting ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Taxol Resistance

Abstract Background Chemoresistance is one of the major obstacles for cancer therapy in the clinic. Circular RNAs (circRNAs) are involved in the pathogenesis of esophageal squamous cell carcinoma (ESCC) and chemoresistance. This study aimed to explore the role and molecular mechanism of circ_0006168 in Taxol resistance of ESCC. Methods The expression levels of circ_0006168, microRNA-194-5p (miR-194-5p) and jumonji domain containing 1C (JMJD1C) were measured by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. The half-inhibition concentration (IC50) value of Taxol was evaluated by Cell Counting Kit-8 (CCK-8) assay. Cell proliferation was evaluated by CCK-8 and colony formation assays. Cell migration and invasion were detected by transwell assay. Cell apoptosis was determined by flow cytometry. The interaction between miR-194-5p and circ_0006168 or JMJD1C was predicted by bioinformatics analysis (Circinteractome and TargetScan) and verified by dual-luciferase reporter and RNA Immunoprecipitation (RIP) and RNA pull-down assays. The mice xenograft model was established to investigate the roles of circ_0006168 in vivo. Results Circ_0006168 and JMJD1C were upregulated and miR-194-5p was downregulated in ESCC tissues, ESCC cells, and Taxol-resistant cells. Functionally, knockdown of circ_0006168 or JMJD1C increased Taxol sensitivity of ESCC in vitro via inhibiting cell proliferation, migration and invasion, and promoting apoptosis. Moreover, circ_0006168 could directly bind to miR-194-5p and JMJD1C was verified as a direct target of miR-194-5p. Mechanically, circ_0006168 was a sponge of miR-194-5p to regulate JMJD1C expression in ESCC cells. Furthermore, JMJD1C overexpression reversed the promotive effect of circ_0006168 knockdown on Taxol sensitivity. Besides, circ_0006168 silence suppressed tumor growth in vivo. Conclusion Circ_0006168 facilitated Taxol resistance in ESCC by regulating miR-194-5p/JMJD1C axis, providing a promising therapeutic target for ESCC chemotherapy.

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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 ◽

10.1186/s12885-021-08779-4 ◽

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.

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MicroRNA-573 inhibits cell proliferation, migration and invasion and is downregulated by PICSAR in cutaneous squamous cell carcinoma

Bosnian Journal of Basic Medical Sciences ◽

10.17305/bjbms.2021.6301 ◽

2021 ◽

Author(s):

Yanhua Wang ◽

Shengjian Tang ◽

Jianping Lv

Keyword(s):

Cell Proliferation ◽

Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Cutaneous Squamous Cell Carcinoma ◽

Cell Counting ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Tumor Tissues ◽

Regulatory Effects

The incidence of cutaneous squamous cell carcinoma (cSCC) has been increasing in recent years. Meanwhile, microRNAs (miRNAs) have been found to play vital roles in various cancers, including cSCC. This study aimed to investigate the expression of microRNA-573 (miR-573) in cSCC, its relationship with long non-coding RNA PICSAR and analyze its biological role. The relationship between PICSAR and miR-573 was confirmed by dual-luciferase reporter assay and Pearson’s correlation coefficient analysis. The levels of PICSAR and miR-573 were measured using quantitative Real-Time PCR. Cell Counting Kit-8 assay was used to evaluate the cSCC cell proliferation ability. The migration and invasion abilities of cSCC cells were evaluated by Transwell assay. PICSAR expression was increased and miR-573 was decreased in tumor tissues and cSCC cell lines. PICSAR and miR-573 can bind directly, and miR-573 expression was downregulated by PICSAR in cSCC. Overexpression of miR-573 significantly inhibited the proliferation, migration and invasion abilities of A431 and SCC13 cells. Additionally, miR-573 overexpression reversed the promotion effects of PICSAR overexpression on cSCC cell proliferation, migration and invasion abilities. In conclusion, our findings indicated that miR-573 expression was decreased in tumor tissues and cSCC cells and was downregulated by PICSAR in cSCC. Additionally, miR-573 overexpression inhibited cSCC cell proliferation, migration and invasion, and reversed the promotion effects of PICSAR overexpression on cSCC cell biological functions. Thus, miR-573 might function as a tumor suppressor and might be involved in the regulatory effects of PICSAR on tumorigenesis in cSCC.

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LncRNA JPX Promotes Esophageal Squamous Cell Carcinoma Progression by Targeting miR-516b-5p/VEGFA Axis

10.21203/rs.3.rs-798922/v1 ◽

2021 ◽

Author(s):

Yi He ◽

Bin Li ◽

Yang Yang ◽

Rong Hua ◽

Zhigang Li

Keyword(s):

Cell Proliferation ◽

Squamous Cell Carcinoma ◽

Esophageal Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Fish Cell

Abstract Background: Long non-coding RNAs (lncRNAs) are reported act as important regulators in various cancers. LncRNA JPX was identified as an oncogenic regulator in lung cancer. However, the function of lncRNA JPX in the progression of esophageal squamous cell carcinoma (ESCC) remains unclear. Methods: The effects and molecular mechanism of JPX on the progression of ESCC were investigated using fluorescence in situ hybridization (FISH), cell proliferation, quantitative real-time PCR (qRT-PCR), western blot, dual luciferase, cell cycle, 5-Ethynyl-2′-Deoxyuridine (EdU) incorporation, transwell, RNA pull-down, tube formation and RNA immunoprecipitation (RIP) assays. Results: In the present study, we found JPX was highly expressed in tissues of ESCC patients and different ESCC cell lines. Functional assays demonstrated that JPX promoted ESCC cell proliferation, migration and invasion in vitro and tumor growth in vivo. Moreover, we found JPX promoted ESCC mobility in vitro. Mechanistically, the results showed that JPX functions as a sponge of miR-516b-5p, which targets an oncogene vascular endothelial growth factor A (VEGFA) in ESCC cells. Interactions between miR-516b-5p and JPX or VEGFA were confirmed by luciferase reporter assays. Furthermore, inhibition of JPX significantly attenuated the cell growth and mobility ability of ESCC cells in vitro. In addition, miR-516b-5p overexpression abrogated JPX enhanced proliferation, migration, invasion, and angiogenesis of ESCC cells. Conclusions: Our study demonstrated that JPX played an important role in promoting ESCC progression via the miR-516b-5p/VEGFA pathway and might serve as a promising novel therapeutic target for ESCC patients.

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MicroRNA-99a-5p suppresses cell proliferation, migration, and invasion by targeting isoprenylcysteine carboxylmethyltransferase in oral squamous cell carcinoma

Journal of International Medical Research ◽

10.1177/0300060520939031 ◽

2021 ◽

Vol 49 (5) ◽

pp. 030006052093903

Author(s):

Xiang Sun ◽

Huixin Yan

Keyword(s):

Cell Proliferation ◽

Squamous Cell Carcinoma ◽

Oral Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Cell Lines ◽

Squamous Cell ◽

Cell Counting ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Isoprenylcysteine Carboxylmethyltransferase

Background MicroRNA (miR)-99a-5p acts as a tumor suppressor in several tumors, including bladder cancer and breast cancer, but its biological function in oral squamous cell carcinoma (OSCC) is poorly understood. Methods miR-99a-5p expression was determined in OSCC tissues and cell lines using quantitative reverse transcription polymerase chain reaction (RT-qPCR). Cell proliferation was assessed by the Cell Counting Kit-8 assay and colony formation assay. Wound healing and Transwell assays were used to analyze migration and invasion abilities, respectively, in OSCC cells. The luciferase reporter assay, RT-qPCR, and western blotting were used to determine the relationship between miR-99a-5p and isoprenylcysteine carboxylmethyltransferase (ICMT). Results miR-99a-5p expression in OSCC tissues and cell lines was significantly decreased compared with corresponding controls, and was significantly associated with clinical stage and lymph node metastasis in OSCC. Functional assays revealed that miR-99a-5p overexpression significantly inhibited the proliferation, migration, and invasion abilities of CAL-27 and TCA-8113 OSCC cells. miR-99a-5p was found to directly target ICMT, while ICMT restoration reversed the role of miR-99a-5p in OSCC cells. Conclusions Our results indicate that miR-99a-5p-mediates the down-regulation of ICMT, which could be used as a novel potential therapeutic target for OSCC treatment.

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LncRNA HOXA-AS3 promotes the progression of oral squamous cell carcinoma via inhibiting miR-218-5p

10.21203/rs.2.22788/v1 ◽

2020 ◽

Author(s):

Yue Zhao ◽

Rui Yao

Keyword(s):

Cell Proliferation ◽

Squamous Cell Carcinoma ◽

Oral Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Colony Formation ◽

Cell Counting ◽

Luciferase Reporter ◽

Gene Assay

Abstract Objective: The aim of the present study was to investigate the roles and molecular mechanism of long non-coding RNA (lncRNA) HOXA-AS3 in the progression of oral squamous cell carcinoma (OSCC). Methods : The expression of HOXA-AS3 and miR-218-5p was detected in OSCC tissues and cells using quantitative real-time polymerase chain reaction (qRT-PCR). Cell Counting Kit-8 (CCK-8) and colony formation assays were used to examine the effects of HOXA-AS3 and miR-218-5p on the proliferation of OSCC cells. Luciferase reporter gene assay was used to confirm the directly binding condition between lncRNA HOXA-AS3 and miR-218-5p in OSCC cells. Subsequently, a tumor xenograft model was used to determine the function of HOXA-AS3 in OSCC growth in vivo . Results: The relative expression of lncRNA HOXA-AS3 was observably upregulated in OSCC tissues and cell lines compared with the para-cancerous tissues and normal human oral keratinocyte (NHOK), respectively. Knockdown of HOXA-AS3 significantly inhibited the cell proliferation and colony formation of OSCC in vitro and in vivo . Bioinformatics and luciferase reporter assays showed that HOXA-AS3 directly bound to miR-218-5p. Moreover, the expression of miR-218-5p was negatively regulated by HOXA-AS3, and there was an inverse correlation between them. Silencing miR-218-5p reversed the inhibitory effect of lncRNA HOXA-AS3 knockdown on the proliferative potential of OSCC cells. Conclusion: In summary, our study illustrated lncRNA HOXA-AS3 promoted cancer cell proliferation in OSCC possibly by inhibiting miR-218-5p for the first time, which provides a new target or a potential diagnostic biomarker of the treatment for OSCC.

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Corilagin Inhibits Esophageal Squamous Cell Carcinoma by Inducing DNA Damage and Down-Regulation of RNF8

Anti-Cancer Agents in Medicinal Chemistry ◽

10.2174/1871520619666190307120811 ◽

2019 ◽

Vol 19 (8) ◽

pp. 1021-1028 ◽

Cited By ~ 3

Author(s):

Fanghua Qiu ◽

Lifang Liu ◽

Yu Lin ◽

Zetian Yang ◽

Feng Qiu

Keyword(s):

Cell Proliferation ◽

Dna Damage ◽

Squamous Cell Carcinoma ◽

Esophageal Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Cell Apoptosis ◽

Cell Counting ◽

Antitumor Effects

Background:Esophageal squamous cell carcinoma (ESCC), the most prevalent histologic subtype of esophageal cancer, is an aggressive malignancy with poor prognosis and a high incidence in the East. Corilagin, an active component present in Phyllanthus niruri L., has been shown to suppress tumor growth in various cancers. However, the effects of corilagin on ESCC and the mechanisms for its tumor suppressive function remain unknown.Methods:Cell proliferation was measured by Cell Counting Kit-8 assay and colony formation assays. Annexin V/PI double-staining was performed to assess cell apoptosis. Immunofluorescence staining and western blotting were used to evaluate the protein expression. A xenograft mice model was used to assess the in vivo antitumor effects of corilagin alone or in combination with cisplatin.Results:We for the first time showed that corilagin was effectively able to inhibit ESCC cell proliferation and induce cell apoptosis. Additionally, our results validated its antitumor effects in vivo using a xenograft mouse model. Mechanistically, we found that corilagin caused significant DNA damage in ESCC cells. We found that corilagin could significantly attenuate the expression of the E3 ubiquitin ligase RING finger protein 8 (RNF8) through ubiquitin-proteasome pathway, leading to the inability of DNA damage repair response and eventually causing cell apoptosis. Furthermore, we also showed that corilagin substantially enhanced the antitumor effects of chemotherapy drug cisplatin both in vitro and in vivo.Conclusion:Our results not only provided novel and previously unrecognized evidences for corilagin-induced tumor suppression through inducing DNA damage and targeting RNF8 in ESCC, but also highlighted that corilagin might serve as an adjunctive treatment to conventional chemotherapeutic drugs in ESCC patients.

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Long Non-Coding RNA CCAT2 Promotes the Development of Esophageal Squamous Cell Carcinoma by Inhibiting miR-200b to Upregulate the IGF2BP2/TK1 Axis

Frontiers in Oncology ◽

10.3389/fonc.2021.680642 ◽

2021 ◽

Vol 11 ◽

Author(s):

Xiaodan Wu ◽

Yihui Fan ◽

Yupeng Liu ◽

Biao Shen ◽

Haimin Lu ◽

...

Keyword(s):

Squamous Cell Carcinoma ◽

Esophageal Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Clinical Samples ◽

Non Coding Rna

Long non-coding RNAs (lncRNAs) have been shown to play important roles in human cancers, including esophageal squamous cell carcinoma (ESCC). In the current study, we identified CCAT2 as a relevant lncRNA and investigated its role in the progression of ESCC. RT-qPCR was adopted to detect CCAT2 expression in collected clinical samples, ESCC cell lines, and a normal cell line. We tested the correlation between CCAT2 expression and the prognosis of ESCC. RT-qPCR or immunoblotting was adopted to detect the expression of relevant factors in ESCC tissues or cells. Cell proliferation, apoptosis, migration, and invasion were examined by colony formation assay, flow cytometry, scratch assay, and Transwell assay, respectively, while subcutaneous tumorigenesis in nude mice was adopted to examine the role of CCAT2 in tumorigenesis of ESCC cells in vivo. Bioinformatics analysis, dual luciferase reporter assay, and RIP were conducted for the target relationship profiling. Me-RIP was adopted to detect m6A modification level of TK1 in ESCC tissues or cells. Upregulated CCAT2, IGF2BP2, and TK1 expression and inhibited miR-200b expression were observed in ESCC cells and tissues. CCAT2 bound to miR-200b and reduced its expression, leading to upregulated IGF2BP2 expression. IGF2BP2 improved TK1 mRNA stability to enhance its expression by recognizing its m6A modification. CCAT2 promoted the migration and invasion of ESCC cells in vitro, and tumorigenesis in vivo by upregulating TK1 expression, while overexpression of miR-200b reversed these effects of CCAT2. Overall, this study suggests that CCAT2 competitively binds to miR-200b to alleviate its inhibitory effects on IGF2BP2 expression, resulting in elevated TK1 expression, and an ensuing promotion of the development of ESCC.

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Circ_DLG1 facilitates esophageal squamous cell carcinoma progression by mediating miR-338-3p/MAP3K9 axis via activating MAPK/ERK pathway

10.21203/rs.3.rs-16608/v1 ◽

2020 ◽

Author(s):

Yixuan Yang ◽

Bing Zhu ◽

Zhaofeng Ning ◽

Xiaodong Wang ◽

Zhaoxia Li ◽

...

Keyword(s):

Cell Cycle ◽

Squamous Cell Carcinoma ◽

Esophageal Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Mitogen Activated Protein Kinase ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Erk Pathway

Abstract Background: Esophageal squamous cell carcinoma (ESCC) is an aggressive malignancy with a high incidence and poor prognosis. The document of circular RNAs (circRNAs) is frequently associated with cancer development. This study intended to explore the functional mechanism of circ_DLG1 in ESCC.Methods: The expression of circ_DLG1, miR-338-3p and Mitogen-Activated Protein Kinase Kinase Kinase 9 (MAP3K9) was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Cell cycle, proliferation, migration and invasion were performed for functional analysis using flow cytometry, 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) and transwell assay, respectively. The protein levels of MAP3K9, p38, phosphor p38 (p-p38), ERK1/2, phosphor ERK1/2 (p-ERK1/2) were detected by western blot. Bioinformatics tool for target prediction used the online tool starBase. Dual-luciferase reporter assay was performed to verify the target relationship. The animal experiments were performed to ascertain the role of circ_DLG1 in vivo.Results: The expression of circ_DLG1 was elevated in ESCC tissues, plasma and cells. Circ_DLG1 knockdown inhibited cell cycle, proliferation, migration and invasion. MAP3K9 was highly expressed in ESCC tissues and cells, and its overexpression rescued the effects of circ_DLG1 knockdown. MiR-338-3p was a link between circ_DLG1 and MAP3K9, and circ_DLG1 regulated the expression of MAP3K9 by targeting miR-338-3p. The MAPK/ERK pathway was involved in the circ_DLG1/miR-338-3p/MAP3K9 regulatory axis. Circ_DLG1 knockdown blocked the tumor growth in vivo by regulating miR-338-3p and MAP3K9.Conclusion: Circ_DLG1 contributed to the malignant progression of ESCC by mediating the miR-338-3p/MAP3K9 axis via activating the MAPK/ERK signaling pathway. This paper provided a novel action mode of circ_DLG1 in ESCC.

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Targeting SKA3 suppresses the proliferation and chemoresistance of laryngeal squamous cell carcinoma via impairing PLK1–AKT axis-mediated glycolysis

Cell Death and Disease ◽

10.1038/s41419-020-03104-6 ◽

2020 ◽

Vol 11 (10) ◽

Author(s):

Wei Gao ◽

Yuliang Zhang ◽

Hongjie Luo ◽

Min Niu ◽

Xiwang Zheng ◽

...

Keyword(s):

Cell Proliferation ◽

Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Laryngeal Squamous Cell Carcinoma ◽

Critical Role ◽

In Vivo Experiments ◽

Potential Strategy

Abstract Spindle and kinetochore-associated complex subunit 3 (SKA3) is a well-known regulator of chromosome separation and cell division, which plays an important role in cell proliferation. However, the mechanism of SKA3 regulating tumor proliferation via reprogramming metabolism is unknown. Here, SKA3 is identified as an oncogene in laryngeal squamous cell carcinoma (LSCC), and high levels of SKA3 are closely associated with malignant progression and poor prognosis. In vitro and in vivo experiments demonstrate that SKA3 promotes LSCC cell proliferation and chemoresistance through a novel role of reprogramming glycolytic metabolism. Further studies reveal the downstream mechanisms of SKA3, which can bind and stabilize polo-like kinase 1 (PLK1) protein via suppressing ubiquitin-mediated degradation. The accumulation of PLK1 activates AKT and thus upregulates glycolytic enzymes HK2, PFKFB3, and PDK1, resulting in enhancement of glycolysis. Furthermore, our data reveal that phosphorylation at Thr360 of SKA3 is critical for its binding to PLK1 and the increase in glycolysis. Collectively, the novel oncogenic signal axis “SKA3-PLK1-AKT” plays a critical role in the glycolysis of LSCC. SKA3 may serve as a prognostic biomarker and therapeutic target, providing a potential strategy for proliferation inhibition and chemosensitization in tumors, especially for LSCC patients with PLK1 inhibitor resistance.

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