Long non-coding RNA CASC2 ameliorates sepsis-induced acute kidney injury by regulating the miR-155 and NF-κB pathway
Sepsis is a systemic inflammatory response syndrome that can cause multiple-organ damage, including acute kidney injury (AKI). Studies have shown that the long non-coding RNA cancer susceptibility candidate 2 (CASC2) is involved in the occurrence and development of multiple human diseases, although...
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| Published in: | International journal of molecular medicine Vol. 45; no. 5; pp. 1554 - 1562 |
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| Main Authors: | , , , , |
| Format: | Journal Article |
| Language: | English |
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D.A. Spandidos
01.05.2020
Spandidos Publications UK Ltd |
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| ISSN: | 1107-3756, 1791-244X, 1791-244X |
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| Abstract | Sepsis is a systemic inflammatory response syndrome that can cause multiple-organ damage, including acute kidney injury (AKI). Studies have shown that the long non-coding RNA cancer susceptibility candidate 2 (CASC2) is involved in the occurrence and development of multiple human diseases, although its expression and role in AKI has not yet been reported. The present study demonstrated that the expression of CASC2 was significantly decreased in the serum of patients with sepsis compared with healthy subjects. In addition, the CASC2 level was negatively associated with the severity of AKI. Further experiments revealed that CASC2 promoted cell viability and inhibited inflammatory factor secretion, apoptosis and oxidative stress in lipopolysaccharide-stimulated human renal tubular epithelial HK-2 cells. Importantly, the current study observed that CASC2 was negatively associated with a pro-inflammatory microRNA (miR)-155. In addition, the upregulation of CASC2 significantly suppressed the nuclear factor κB (NF-κB) signaling pathway. In conclusion, the results of the present study suggested that CASC2 may serve as a potential target for treating sepsis-induced AKI by inhibiting the miR-155 and NF-κB pathway-mediated inflammation. |
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| AbstractList | Sepsis is a systemic inflammatory response syndrome that can cause multiple-organ damage, including acute kidney injury (AKI). Studies have shown that the long non-coding RNA cancer susceptibility candidate 2 (CASC2) is involved in the occurrence and development of multiple human diseases, although its expression and role in AKI has not yet been reported. The present study demonstrated that the expression of CASC2 was significantly decreased in the serum of patients with sepsis compared with healthy subjects. In addition, the CASC2 level was negatively associated with the severity of AKI. Further experiments revealed that CASC2 promoted cell viability and inhibited inflammatory factor secretion, apoptosis and oxidative stress in lipopolysaccharide-stimulated human renal tubular epithelial HK-2 cells. Importantly, the current study observed that CASC2 was negatively associated with a pro-inflammatory microRNA (miR)-155. In addition, the upregulation of CASC2 significantly suppressed the nuclear factor κB (NF-κB) signaling pathway. In conclusion, the results of the present study suggested that CASC2 may serve as a potential target for treating sepsis-induced AKI by inhibiting the miR-155 and NF-κB pathway-mediated inflammation. Sepsis is a systemic inflammatory response syndrome that can cause multiple‑organ damage, including acute kidney injury (AKI). Studies have shown that the long non‑coding RNA cancer susceptibility candidate 2 (CASC2) is involved in the occurrence and development of multiple human diseases, although its expression and role in AKI has not yet been reported. The present study demonstrated that the expression of CASC2 was significantly decreased in the serum of patients with sepsis compared with healthy subjects. In addition, the CASC2 level was negatively associated with the severity of AKI. Further experiments revealed that CASC2 promoted cell viability and inhibited inflammatory factor secretion, apoptosis and oxidative stress in lipopolysaccharide‑stimulated human renal tubular epithelial HK‑2 cells. Importantly, the current study observed that CASC2 was negatively associated with a pro‑inflammatory microRNA (miR)‑155. In addition, the upregulation of CASC2 significantly suppressed the nuclear factor κB (NF‑κB) signaling pathway. In conclusion, the results of the present study suggested that CASC2 may serve as a potential target for treating sepsis‑induced AKI by inhibiting the miR‑155 and NF‑κB pathway‑mediated inflammation.Sepsis is a systemic inflammatory response syndrome that can cause multiple‑organ damage, including acute kidney injury (AKI). Studies have shown that the long non‑coding RNA cancer susceptibility candidate 2 (CASC2) is involved in the occurrence and development of multiple human diseases, although its expression and role in AKI has not yet been reported. The present study demonstrated that the expression of CASC2 was significantly decreased in the serum of patients with sepsis compared with healthy subjects. In addition, the CASC2 level was negatively associated with the severity of AKI. Further experiments revealed that CASC2 promoted cell viability and inhibited inflammatory factor secretion, apoptosis and oxidative stress in lipopolysaccharide‑stimulated human renal tubular epithelial HK‑2 cells. Importantly, the current study observed that CASC2 was negatively associated with a pro‑inflammatory microRNA (miR)‑155. In addition, the upregulation of CASC2 significantly suppressed the nuclear factor κB (NF‑κB) signaling pathway. In conclusion, the results of the present study suggested that CASC2 may serve as a potential target for treating sepsis‑induced AKI by inhibiting the miR‑155 and NF‑κB pathway‑mediated inflammation. Sepsis is a systemic inflammatory response syndrome that can cause multiple‑organ damage, including acute kidney injury (AKI). Studies have shown that the long non‑coding RNA cancer susceptibility candidate 2 (CASC2) is involved in the occurrence and development of multiple human diseases, although its expression and role in AKI has not yet been reported. The present study demonstrated that the expression of CASC2 was significantly decreased in the serum of patients with sepsis compared with healthy subjects. In addition, the CASC2 level was negatively associated with the severity of AKI. Further experiments revealed that CASC2 promoted cell viability and inhibited inflammatory factor secretion, apoptosis and oxidative stress in lipopolysaccharide‑stimulated human renal tubular epithelial HK‑2 cells. Importantly, the current study observed that CASC2 was negatively associated with a pro‑inflammatory microRNA (miR)‑155. In addition, the upregulation of CASC2 significantly suppressed the nuclear factor κB (NF‑κB) signaling pathway. In conclusion, the results of the present study suggested that CASC2 may serve as a potential target for treating sepsis‑induced AKI by inhibiting the miR‑155 and NF‑κB pathway‑mediated inflammation. |
| Author | Shang, Futai Wang, Min Ji, Ting Wei, Jilou Zang, Kui |
| Author_xml | – sequence: 1 givenname: Min surname: Wang fullname: Wang, Min – sequence: 2 givenname: Jilou surname: Wei fullname: Wei, Jilou – sequence: 3 givenname: Futai surname: Shang fullname: Shang, Futai – sequence: 4 givenname: Kui surname: Zang fullname: Zang, Kui – sequence: 5 givenname: Ting surname: Ji fullname: Ji, Ting |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32323747$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_3389_fphys_2022_932693 crossref_primary_10_3389_fphar_2025_1570000 crossref_primary_10_1038_s41598_024_79367_2 crossref_primary_10_1155_2022_6291497 crossref_primary_10_3389_fphys_2022_849403 crossref_primary_10_3389_fphys_2022_830924 crossref_primary_10_1186_s40246_024_00578_9 crossref_primary_10_1038_s41598_024_81212_5 crossref_primary_10_3389_fimmu_2021_722004 crossref_primary_10_3389_fimmu_2021_798713 crossref_primary_10_3389_fcimb_2021_563126 crossref_primary_10_3389_fphar_2025_1627253 crossref_primary_10_1155_2022_5845627 |
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| SubjectTerms | acute kidney injury Acute Kidney Injury - genetics Adult Aged Animals Apoptosis Apoptosis - genetics Cancer cancer susceptibility candidate 2 Cell growth Cell Line Cell Survival - genetics Down-Regulation - genetics Female Gene Expression Regulation, Neoplastic - genetics HEK293 Cells Humans Inflammation - genetics Kidneys Laboratory animals long non-coding RNA Male Males Mice Mice, Inbred BALB C microRNA-155 MicroRNAs MicroRNAs - genetics Middle Aged NF-kappa B - genetics nuclear factor-κB Oxidative Stress - genetics Sepsis Sepsis - genetics Tumor necrosis factor-TNF Tumor Suppressor Proteins - genetics Up-Regulation - genetics Young Adult |
| Title | Long non-coding RNA CASC2 ameliorates sepsis-induced acute kidney injury by regulating the miR-155 and NF-κB pathway |
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