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tients. The result showed that CZ Score had a better value for prognostic evaluation and surgical decision-making as compared with the other scoring systems.

miRNA-105 has been reported in a vast number of malignancies, including hepatocellular carcinoma and colorectal, esophageal, breast and non-small lung cancers. Still, the biological role of miR-105 remains mostly uncovered in oral squamous cell carcinoma (OSCC).

miR-105 expression in OSCC tissues and cell lines was detected by qRT-PCR. Survival analysis was performed using the Kaplan-Meier method, while the prognostic significance of miR-105 was evaluated by Cox regression analysis with a cohort of 90 OSCC patients. The effects of miR-105 on the proliferation of tumor cells were analyzed by CCK-8 assay and crystal violet staining, while cell invasion was assessed by transwell assays.

Our current work indicates that miR-105 was upregulated in human OSCC tissues and cell lines. Moreover, miR-105 expression was closely associated with tumor size as well as clinical and differentiation stages. Notably, an elevated expression of miR-105 may predict some poor clinical prognosis in OSCC patients. Furthermore, miR-105 overexpression can significantly promote the proliferation and invasion of OSCC cells, whereas downregulation of miR-105 inhibits these cellular events.

This study demonstrates that miR-105 can promote the proliferation and invasion of OSCC cells. High expression of miR-105 predicts poor prognosis for OSCC and, therefore, it may represent a prognostic biomarker and putative therapeutic target for patients affected by OSCC.

This study demonstrates that miR-105 can promote the proliferation and invasion of OSCC cells. (S)-2-Hydroxysuccinic acid High expression of miR-105 predicts poor prognosis for OSCC and, therefore, it may represent a prognostic biomarker and putative therapeutic target for patients affected by OSCC.

Skeletal metastases are a common problem in breast cancer patients. Identifying new prognostic factors can improve survival estimations and guide healthcare professionals in therapeutic decision-making. Our study aimed to determine the prognostic value of inflammatory biomarkers such as neutrophil-to-lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR), and C-reactive protein/albumin ratio (CAR) in patients with breast cancer skeletal metastases.

Clinical data from 212 patients with breast cancer skeletal metastases were retrospectively analyzed. The optimal cut-off values of each inflammatory biomarker were extracted from the receiver operating characteristic (ROC) curves. Patients were divided into high-value and low-value groups according to the cut-off values of NLR, LMR, and CAR. We investigated the relationship between inflammatory biomarkers and clinicopathological characteristics. The Kaplan-Meier method was used to measure progression-free survival (PFS) and overall survival (OS). The survitients of breast cancer skeletal metastases.

LMR less then 3.43 and NLR≥2.48 were independently associated with worse prognosis of patients of breast cancer skeletal metastases.

Prostate cancer threatens the life and health of men in China. Desmocollin-2 (

) is a member of

family, abnormal expression of which can affect the invasion and metastasis of tumor cells. The aim of this study was to investigate the role of

in prostate cancer.

Regulating

expression in prostate cancer cells was conducted with transfection. The expression of

, apoptosis-related proteins, cell cycle-related proteins and E-cadherin (E-cad)/β-catenin pathway was detected by Western blot analysis. The proliferation, clone formation ability, migration, invasion and apoptosis of transfected cells were in turn detected by cell counting kit-8 (CCK-8) assay, clone formation assay, wound healing assay, transwell assay and flow cytometry analysis.

expression was increased in prostate cancer cells compared with RWPE-1 cells. Inhibition of

promoted the proliferation, clone formation ability, migration and invasion while suppressed apoptosis of LNCaP cells and PC-3 cells. Inhibition of

affected the expression of apoptosis-related proteins and cell cycle-related proteins according to the changes of apoptosis and proliferation. Furthermore, inhibition of

up-regulated the expression of p-β-catenin and EGFR while down-regulated the expression of E-cad.

overexpression exerted the opposite effect of inhibition of

on LNCaP cells and PC-3 cells.

expression was increased in prostate cancer cells. In addition, inhibition of

promoted the proliferation, clone formation ability, migration and invasion while suppressed apoptosis of LNCaP cells and PC-3 cells, which provided the fundamental basis for treatment of prostate cancer.

DSC2 expression was increased in prostate cancer cells. In addition, inhibition of DSC2 promoted the proliferation, clone formation ability, migration and invasion while suppressed apoptosis of LNCaP cells and PC-3 cells, which provided the fundamental basis for treatment of prostate cancer.

Long noncoding RNAs (lncRNAs) play essential functions in the development of several cancers, including colorectal cancer (CRC). Nevertheless, how PCAT18 regulates CRC tumorigenesis remains unclear. In this research, we aimed to investigate the roles of PCAT18 in CRC.

qRT-PCR and Western blot were used to analyze RNA and protein levels. CCK8, colony formation, transwell and wound healing assays were utilized to analyze proliferation, migration and invasion. Luciferase reporter assay was used to analyze RNA interactions.

PCAT18 was found to be highly expressed in CRC tissues and cells. PCAT18 level was positively correlated with lymph node metastasis and TNM stage. Functionally, PCAT18 silencing induced impairment of CRC proliferation, migration and invasion. Besides, PCAT18 was identified to inhibit miR-759. PCAT18 promotes SPRR3 expression through binding to miR-759. Furthermore, miR-759 inhibitors or SPRR3 ectopic expression partially rescued the abilities of proliferation, migration and invasion in CRC cells transfected with sh-PCAT18.

Therefore, our study demonstrated that PCAT18 contributes to CRC progression through regulating miR-759/SPRR3 axis, which provides a new theoretical basis of explaining CRC tumorigenesis.

Therefore, our study demonstrated that PCAT18 contributes to CRC progression through regulating miR-759/SPRR3 axis, which provides a new theoretical basis of explaining CRC tumorigenesis.