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Introduction LncRNAs have been reported to play critical roles in liver cancer, while its role in other cancers remains unclear. The aim of this study was to investigate the role of DCST1-AS1 in cervical squamous cell carcinoma (CSCC). Methods Expression of DCST1-AS1 in CSCC tissues and non-tumor tissues from 68 CSCC patients was determined by RT-qPCR. A 5-year follow-up study was carried out to explore the prognostic value of DCST1-AS1 for CSCC. Overexpression of DCST1-AS1 and miR-107 was achieved in CSCC tissues to explore the interaction between them. The roles of DCST1-AS1, miR-107 and CDK6 in regulating the proliferation and viability of CSCC cells were assessed by cell proliferation and viability assays, respectively. Results We found that DCST1-AS1 was upregulated in CSCC and predicted poor survival. RNA interaction prediction showed potential interaction between DCST1-AS1 and miR-107. However, overexpression experiments revealed no significant interaction between them. Moreover, overexpression of DCST1-AS1 led to upregulate CDK6 and increase cell proliferation rate, while overexpression of miR-107 played an opposite role and attenuate the effects of overexpression of DCST1-AS1. Conclusion DCST1-AS1 may sponge miR-107 to upregulate CDK6 in CSCC.

Introduction The purpose of this study is to investigate the role of long non-coding RNA (lncRNA) miR503 Host Gene (miR503HG) in cervical squamous cell carcinoma (CSCC). Methods Analysis of TCGA dataset revealed that expression levels of miR503HG in CSCC tissues were over 12 times lower than those in non-tumor tissues, indicating its involvement in CSCC. Results In this study, we observed that levels of miR503HG in plasma were significantly lower in CSCC patients than in healthy participants. The cisplatin-based treatment further downregulated miR503HG in both patients and CSCC cells. MiR503HG overexpression in CSCC cells led to the suppression of miR-155 and elevation of Caspase-3, acting as the downstream target of miR-155. Cell apoptosis analysis showed that miR503HG and Caspase-3 overexpression led to an increased cell apoptosis rate under Cisplatin treatment. MiR-155 played the opposite role and attenuated the functions of Caspase-3 and miR503HG overexpression. Conclusion Therefore, miR503HG may regulate the drug resistance of CSCC cells by regulating mir-155/Caspase-3.

Huizhen Zhang,1 Shuangling Jin,1 Aifang Ji,2 Ying Ma,3 Chunyan Zhang,1 Ailan Wang,1 Rui Wang1 1Department of Gynecology, Heping Hospital Affiliated to Changzhi Medical College, Changzi, Shanxi Province, 046000, People’s Republic of China; 2Department of Clinical Laboratory, Heping Hospital Affiliated to Changzhi Medical College, Changzi, Shanxi Province, 046000, People’s Republic of China; 3Department of Obstetrics, Heping Hospital Affiliated to Changzhi Medical College, Changzi, Shanxi Province, 046000, People’s Republic of ChinaCorrespondence: Shuangling JinDepartment of Gynecology, Heping Hospital Affiliated to Changzhi Medical College, Changzhi City, Shanxi Province, 046000, People’s Republic of ChinaEmail nj6077@163.comBackground: SLC16A1-AS1 has been characterized as an oncogenic long non-coding (lncRNA) in breast cancer and bladder cancer, while its role in cervical squamous cell carcinoma (CSCC) is unknown.Methods: CSCC and non-tumor tissue samples were collected from 60 female patients, and qPCR was performed to detect the expression of SLC16A1-AS1, miR-194 and SOCS2. Luciferase reporter assay was performed to detect the interaction between SLC16A1-AS1 and miR-194. Colony formation assay was used to detect cell proliferation.Results: SLC16A1-AS1 was down-regulated in CSCC and correlated with poor survival. Overexpression of SLC16A1-AS1 could inhibit the proliferation of cervical cancer cells. In addition, SLC16A1-AS1 could sponge miR-194 and increase the expression levels of SOCS2, ultimately inhibiting the proliferation of cervical cancer cells.Conclusion: SLC16A1-AS1 was downregulated in CSCC and suppressed cell proliferation in cervical squamous cell carcinoma (CSCC) through the miR-194/SOCS2 axis.Keywords: cervical squamous cell carcinoma, SLC16A1-AS1, miR-194, SOCS2

Introduction LncRNAs have been reported to play critical roles in liver cancer, while its role in other cancers remains unclear. The aim of this study was to investigate the role of DCST1-AS1 in cervical squamous cell carcinoma (CSCC). Methods Expression of DCST1-AS1 in CSCC tissues and non-tumor tissues from 68 CSCC patients was determined by RT-qPCR. A 5-year follow-up study was carried out to explore the prognostic value of DCST1-AS1 for CSCC. Overexpression of DCST1-AS1 and miR-107 was achieved in CSCC tissues to explore the interaction between them. The roles of DCST1-AS1, miR-107 and CDK6 in regulating the proliferation and viability of CSCC cells were assessed by cell proliferation and viability assays, respectively. Results We found that DCST1-AS1 was upregulated in CSCC and predicted poor survival. RNA interaction prediction showed potential interaction between DCST1-AS1 and miR-107. However, overexpression experiments revealed no significant interaction between them. Moreover, overexpression of DCST1-AS1 led to upregulate CDK6 and increase cell proliferation rate, while overexpression of miR-107 played an opposite role and attenuate the effects of overexpression of DCST1-AS1. Conclusion DCST1-AS1 may sponge miR-107 to upregulate CDK6 in CSCC.

Introduction The purpose of this study is to investigate the role of long non-coding RNA (lncRNA) miR503 Host Gene (miR503HG) in cervical squamous cell carcinoma (CSCC). Methods Analysis of TCGA dataset revealed that expression levels of miR503HG in CSCC tissues were over 12 times lower than those in non-tumor tissues, indicating its involvement in CSCC. Results In this study, we observed that levels of miR503HG in plasma were significantly lower in CSCC patients than in healthy participants. The cisplatin-based treatment further downregulated miR503HG in both patients and CSCC cells. MiR503HG overexpression in CSCC cells led to the suppression of miR-155 and elevation of Caspase-3, acting as the downstream target of miR-155. Cell apoptosis analysis showed that miR503HG and Caspase-3 overexpression led to an increased cell apoptosis rate under Cisplatin treatment. MiR-155 played the opposite role and attenuated the functions of Caspase-3 and miR503HG overexpression. Conclusion Therefore, miR503HG may regulate the drug resistance of CSCC cells by regulating mir-155/Caspase-3.

Introduction The incidence of cervical squamous cell carcinoma (CSCC) has expanded in recent years. However, the function of long non-coding RNA (lncRNA) MAGI2-AS3 in the occurrence and progression of CSCC remains unclear. Therefore, the role of lncRNA MAGI2-AS3 in cervical squamous cell carcinoma (CSCC) was investigated in our study. Methods We used qRT-PCR analysis to identify the level of MAGI2-AS3 mRNA expression in CSCC clinical samples and cell lines. We investigated cell migration and invasion of CSCC cells transfected with MAGI2-AS3, miR-233 mimic, or EPB41L3 with transwell assays. Bioinformatics analysis and a luciferase reporter assay were employed to predict the interaction between MAGI2-AS3 and miR-233. Results We found that MAGI2-AS3 and EPB41L3 were both downregulated in CSCC and the expression of this two was positively correlated. Bioinformatics analysis showed that MAGI2-AS3 might bind to miR-233, which could directly target EPB41L3. In CSCC cells, overexpression of MAGI2-AS3 led to upregulated, while overexpression of miRNA-233 led to downregulated expression of EPB41L3. However, MAGI2-AS3 and miR-233 did not affect the expression of each other. In addition, overexpression of MAGI2-AS3 and EPB41L3 led to inhibited cancer cell invasion and migration, while overexpression of miR-233 played an opposite role and attenuated the effects of overexpressing MAGI2-AS3. Conclusion MAGI2-AS3 may sponge miR-233 to upregulate EPB41L3, thereby inhibiting CSCC cell invasion and migration.