Abstract:A long non-coding RNA (lncRNA) called prostate cancer-associated non-coding RNA 1 (PRNCR1) serves crucial roles in the aggressive phenotypes of colorectal cancer and non-small cell lung cancer. However, there is little research on the expression profile, clinical value and detailed functions of PRNCR1 in tongue squamous cell carcinoma (TScc). The aim of the present study was to determine PRNCR1 expression in TScc and to examine the involvement of PRNCR1 in TScc progression. The molecular mechanisms behind the … Show more
“…Knockdown of TUG1 suppressed cisplatin resistance to CAL27/CDDP and SCC25/CDDP cells via modulating CXCR4 and miR‐133b. Lin et al 36 noted that PRNCR1 played as one oncogenic lncRNA gene in the development of TSCC via regulating HOXB5/ miR‑944. Yan et al 37 suggested that knockdown of PCAT‐1 suppressed metastasis of proliferation of TSCC cell through up‐regulating P21.…”
Growing lncRNAs have been noted to involve in the initiation and development of several tumours including tongue squamous cell carcinomas (TSCCs). However, the biological role and mechanism of lncRNA RPSAP52 were not well‐explained. We indicated that RPSAP52 was higher in TSCC samples compared with that in control samples. The higher expression of RPSAP52 was positively correlated with higher T stage and TNM stage. Ectopic expression of RPSAP52 induced TSCC cell growth and cycle and induced cytokine secretion including IFN‐γ, IL‐1β and IL‐6, IL‐8, IL‐10 and TGF‐β. We found that the overexpression of RPSAP52 suppressed miR‐423‐5p expression in SCC‐4 cell. miR‐423‐5p was lower in TSCC samples compared with that in control samples, and miR‐423‐5p level was negatively correlated with higher T stage and TNM stage. Pearson's correlation indicated that miR‐423‐5p was negatively associated with that of RPSAP52 in TSCC tissues. Furthermore, MYBL2 was one direct gene of miR‐423‐5p and elevated expression of miR‐423‐5p suppressed MYBL2 expression and ectopic expression of RPSAP52 increased MYBL2 expression in SCC‐4 cell. Finally, we illustrated that RPSAP52 overexpression promoted TSCC cell growth and cycle and induced cytokine secretion including IFN‐γ, IL‐1β and IL‐6, IL‐8, IL‐10 and TGF‐β via modulating MYBL2. These data provided new insight into RPSAP52, which may be one potential treatment target for TSCC.
“…Knockdown of TUG1 suppressed cisplatin resistance to CAL27/CDDP and SCC25/CDDP cells via modulating CXCR4 and miR‐133b. Lin et al 36 noted that PRNCR1 played as one oncogenic lncRNA gene in the development of TSCC via regulating HOXB5/ miR‑944. Yan et al 37 suggested that knockdown of PCAT‐1 suppressed metastasis of proliferation of TSCC cell through up‐regulating P21.…”
Growing lncRNAs have been noted to involve in the initiation and development of several tumours including tongue squamous cell carcinomas (TSCCs). However, the biological role and mechanism of lncRNA RPSAP52 were not well‐explained. We indicated that RPSAP52 was higher in TSCC samples compared with that in control samples. The higher expression of RPSAP52 was positively correlated with higher T stage and TNM stage. Ectopic expression of RPSAP52 induced TSCC cell growth and cycle and induced cytokine secretion including IFN‐γ, IL‐1β and IL‐6, IL‐8, IL‐10 and TGF‐β. We found that the overexpression of RPSAP52 suppressed miR‐423‐5p expression in SCC‐4 cell. miR‐423‐5p was lower in TSCC samples compared with that in control samples, and miR‐423‐5p level was negatively correlated with higher T stage and TNM stage. Pearson's correlation indicated that miR‐423‐5p was negatively associated with that of RPSAP52 in TSCC tissues. Furthermore, MYBL2 was one direct gene of miR‐423‐5p and elevated expression of miR‐423‐5p suppressed MYBL2 expression and ectopic expression of RPSAP52 increased MYBL2 expression in SCC‐4 cell. Finally, we illustrated that RPSAP52 overexpression promoted TSCC cell growth and cycle and induced cytokine secretion including IFN‐γ, IL‐1β and IL‐6, IL‐8, IL‐10 and TGF‐β via modulating MYBL2. These data provided new insight into RPSAP52, which may be one potential treatment target for TSCC.
“…miR-326 (sponging) i. HOXB5 over-expression ii. FSCN-1 over-expression Prognostic Lin et al ( 2020 ); Liu et al ( 2021 ) Colorectal cancer Over expression Proliferation (↑) Migration (–) Invasion (–) apoptosis (–) N/A N/A Diagnostic Prognostic Yang et al ( 2016 ) NSCLC non-small cell lung carcinoma; OSSCC oral squamous cell carcinoma; EMT epithelial-to-mesenchymal transition ↑: positive impact; ↓: negative impact; –: no effect; N/A: data not available Fig. 3 Summarized information on functional mechanism of PRNCR1 in oncogenesis.…”
Section: Introductionmentioning
confidence: 99%
“…In oral squamous cell carcinoma (OSCC) and tongue squamous cell carcinoma (TSCC), the most common type of OSCC, PRNCR1 over-expression was reported in primary tumors as well as in cancer cell lines (Liu et al 2021 ; Lin et al 2020 ). Following PRNCR1 knockdown reduced tumor phenotypes of cancer cells like proliferation, migration, and invasion suggested the association of the lncRNA in disease pathogenesis.…”
Section: Introductionmentioning
confidence: 99%
“…Following PRNCR1 knockdown reduced tumor phenotypes of cancer cells like proliferation, migration, and invasion suggested the association of the lncRNA in disease pathogenesis. Moreover after PRNCR1 knockdown, TSCC cells also showed increased apoptosis in vitro and reduced growth in tumor xenograft (Lin et al 2020 ).…”
Section: Introductionmentioning
confidence: 99%
“…Thus, over-expression of miR-326 and subsequent down-regulation of FSCN-1 in oral tumor seemed to be an effective strategy of disease management and this might be achieved through targeting PRNCR1 by novel therapeutic measures. In TSCC cells, PRNCR1 was found to attenuate mir-944 and thereby up-regulate expression of HOXB5 (Lin et al 2020 ), a transcription factor over-expressed in head and neck tumors; also in oral cells, HOXB5 was found to involve in the transcriptional up-regulation of EGFR and thereby mediate the activation of AKT/Wnt/β-catenin signaling axis (Lee et al 2020 ) associated with the cell cycle regulation (Vadlakonda et al 2013 ). Moreover, although tumor-suppressive role of miR-944 was reported in breast and colorectal cancers (Flores-Pérez et al 2016 ; Wen et al 2017 ), the miRNA was found to be over-expressed and play an oncogenic role in cervical carcinoma (Park et al 2019 ) and interestingly in tobacco-induced oral cancer (Peng et al 2020 ).…”
Oral cancer (OC) is the most prevalent subtype of cancer arising in the head and neck region. OC risk is mainly attributed to behavioral risk factors such as exposure to tobacco and excessive alcohol consumption, and a lesser extent to viral infections such as human papillomaviruses and Epstein-Barr viruses. In addition to these acquired risk factors, heritable genetic factors have shown to be associated with OC risk. Despite the high incidence, biomarkers for OC diagnosis are lacking and consequently, patients are often diagnosed in advanced stages. This delay in diagnosis is reflected by poor overall outcomes of OC patients, where 5-year overall survival is around 50%. Among the biomarkers proposed for cancer detection, noncoding RNA (ncRNA) can be considered as one of the most promising categories of biomarkers due to their role in virtually all cellular processes. Similar to other cancer types, changes in expressions of ncRNAs have been reported in OC and a number of ncRNAs have diagnostic, prognostic, and therapeutic potential. Moreover, some
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