Expression of Long Nonencoding Ribonucleic Acid SNHG20 in Colon Cancer Tissue in Its Influences on Chemotherapeutic Sensitivity of Colon Cancer Cells
Noncoding RNA (ncRNA) is a kind of RNA that plays a key role in a variety of biological processes, illnesses, and tumours despite the fact that it cannot be translated into proteins. The HT29 colon cancer cell line was utilized to create a 5-FU drug-resistant cell strain (control group), a lentiviru...
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| description | Noncoding RNA (ncRNA) is a kind of RNA that plays a key role in a variety of biological processes, illnesses, and tumours despite the fact that it cannot be translated into proteins. The HT29 colon cancer cell line was utilized to create a 5-FU drug-resistant cell strain (control group), a lentivirus SNHG20 carrier (OE-SNHG20 group), and an SNHG20 shRNA carrier (SNHG20 shRNA carrier group) (SE-SNHG20 group). To determine the expression of cell SNHG20, a real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was utilized, and cholecystokinin-octapeptide (CCK-8) was used to detect the difference in 5-FU inhibitory concentration 50. The goal of the study was to see how variations in long nonencoding ribonucleic acid (lncRNA) SNHG20 expression affect colon cancer cell 5-fluorouracil (5-FU) chemotherapeutic sensitivity by collecting colon cancer and normal para cancer tissues and analysing the differences in SNHG20 expression. The ability of cell cladogenesis was tested using platform cladogenesis. Cell apoptosis was detected using flow cytometry. Western blots revealed the presence of protein phosphatidylinositol kinase (PI3K), protein kinase B (AKT), caspase-3, e-cadherin, and matrix metalloproteinase 9 (MMP-9) enzymes. The findings revealed that SNHG20 expression was considerably upregulated (P |
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The HT29 colon cancer cell line was utilized to create a 5-FU drug-resistant cell strain (control group), a lentivirus SNHG20 carrier (OE-SNHG20 group), and an SNHG20 shRNA carrier (SNHG20 shRNA carrier group) (SE-SNHG20 group). To determine the expression of cell SNHG20, a real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was utilized, and cholecystokinin-octapeptide (CCK-8) was used to detect the difference in 5-FU inhibitory concentration 50. The goal of the study was to see how variations in long nonencoding ribonucleic acid (lncRNA) SNHG20 expression affect colon cancer cell 5-fluorouracil (5-FU) chemotherapeutic sensitivity by collecting colon cancer and normal para cancer tissues and analysing the differences in SNHG20 expression. The ability of cell cladogenesis was tested using platform cladogenesis. Cell apoptosis was detected using flow cytometry. Western blots revealed the presence of protein phosphatidylinositol kinase (PI3K), protein kinase B (AKT), caspase-3, e-cadherin, and matrix metalloproteinase 9 (MMP-9) enzymes. The findings revealed that SNHG20 expression was considerably upregulated (P<0.05) in colon cancer tissue and 5-FU drug-resistant colon cancer cells. Cell 5-FU IC50, cell cladogenesis, cell survival rate, and MMP-9, P-PI3K, and P-AKT expression were all significantly improved. Cell apoptosis and expressions of E-cadherin and caspase-3, on the other hand, were considerably decreased (P<0.05). Cell 5-FU IC50, cell cladogenesis, cell survival rate, and the expressions of MMP-9, P-PI3K, and P-AKT were all significantly lower in the SE-SNHG20 group, although cell apoptosis and the expressions of E-cadherin and caspase-3 were significantly higher (P<0.05). The results revealed that lncRNA SNHG20 could inhibit the chemotherapeutic sensitivity of colon cancer cells to 5-FU by regulating PI3K/AKT pathways. The inhibition of lncRNA SNHG20 expression could promote the apoptosis and proliferation of 5-FU-resistant colon cancer cells.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2022/4752782</identifier><identifier>PMID: 35915794</identifier><language>eng</language><publisher>United States: Hindawi</publisher><subject>1-Phosphatidylinositol 3-kinase ; 5-Fluorouracil ; AKT protein ; Antibodies ; Apoptosis ; Apoptosis - genetics ; Biological activity ; Breast cancer ; Cadherins - genetics ; Cadherins - metabolism ; Cancer ; Caspase 3 - metabolism ; Caspase-3 ; Cell culture ; Cell division ; Cell growth ; Cell Line, Tumor ; Cell Proliferation ; Cell survival ; Chemotherapy ; Cholecystokinin ; Colon ; Colon cancer ; Colonic Neoplasms - drug therapy ; Colonic Neoplasms - genetics ; Colonic Neoplasms - pathology ; Colorectal cancer ; Drug resistance ; Drug sensitization ; Drug therapy ; E-cadherin ; Flow cytometry ; Fluorouracil - pharmacology ; Fluorouracil - therapeutic use ; Gastric cancer ; Gelatinase B ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genetic aspects ; Health aspects ; Humans ; Kinases ; Matrix metalloproteinase ; Matrix Metalloproteinase 9 - metabolism ; Matrix metalloproteinases ; Medical research ; Metalloproteinase ; Metastasis ; Non-coding RNA ; Oncology, Experimental ; Ovarian cancer ; Phosphatidylinositol 3-Kinases - genetics ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphatidylinositol kinase ; Physiological aspects ; Polymerase chain reaction ; Proteins ; Proto-Oncogene Proteins c-akt - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; Reagents ; Reverse transcription ; Ribonucleic acid ; RNA ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; RNA, Small Interfering ; Survival ; Tissue analysis ; Tissues ; Tumors ; Viruses ; Western blotting</subject><ispartof>BioMed research international, 2022, Vol.2022 (1), p.4752782</ispartof><rights>Copyright © 2022 Wenbin Cao et al.</rights><rights>COPYRIGHT 2022 John Wiley & Sons, Inc.</rights><rights>Copyright © 2022 Wenbin Cao et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2022 Wenbin Cao et al. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c476t-faef0813b14d1c6da9747d686a5a441f78e52821c7d00acc7ced86a31f0c3cf83</citedby><cites>FETCH-LOGICAL-c476t-faef0813b14d1c6da9747d686a5a441f78e52821c7d00acc7ced86a31f0c3cf83</cites><orcidid>0000-0001-6364-1241</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9338858/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9338858/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4009,27902,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35915794$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Shah, Shahid Ali</contributor><contributor>Shahid Ali Shah</contributor><creatorcontrib>Cao, Wenbin</creatorcontrib><creatorcontrib>Zhang, Bo</creatorcontrib><creatorcontrib>Liu, Yang</creatorcontrib><title>Expression of Long Nonencoding Ribonucleic Acid SNHG20 in Colon Cancer Tissue in Its Influences on Chemotherapeutic Sensitivity of Colon Cancer Cells</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>Noncoding RNA (ncRNA) is a kind of RNA that plays a key role in a variety of biological processes, illnesses, and tumours despite the fact that it cannot be translated into proteins. The HT29 colon cancer cell line was utilized to create a 5-FU drug-resistant cell strain (control group), a lentivirus SNHG20 carrier (OE-SNHG20 group), and an SNHG20 shRNA carrier (SNHG20 shRNA carrier group) (SE-SNHG20 group). To determine the expression of cell SNHG20, a real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was utilized, and cholecystokinin-octapeptide (CCK-8) was used to detect the difference in 5-FU inhibitory concentration 50. The goal of the study was to see how variations in long nonencoding ribonucleic acid (lncRNA) SNHG20 expression affect colon cancer cell 5-fluorouracil (5-FU) chemotherapeutic sensitivity by collecting colon cancer and normal para cancer tissues and analysing the differences in SNHG20 expression. The ability of cell cladogenesis was tested using platform cladogenesis. Cell apoptosis was detected using flow cytometry. Western blots revealed the presence of protein phosphatidylinositol kinase (PI3K), protein kinase B (AKT), caspase-3, e-cadherin, and matrix metalloproteinase 9 (MMP-9) enzymes. The findings revealed that SNHG20 expression was considerably upregulated (P<0.05) in colon cancer tissue and 5-FU drug-resistant colon cancer cells. Cell 5-FU IC50, cell cladogenesis, cell survival rate, and MMP-9, P-PI3K, and P-AKT expression were all significantly improved. Cell apoptosis and expressions of E-cadherin and caspase-3, on the other hand, were considerably decreased (P<0.05). Cell 5-FU IC50, cell cladogenesis, cell survival rate, and the expressions of MMP-9, P-PI3K, and P-AKT were all significantly lower in the SE-SNHG20 group, although cell apoptosis and the expressions of E-cadherin and caspase-3 were significantly higher (P<0.05). The results revealed that lncRNA SNHG20 could inhibit the chemotherapeutic sensitivity of colon cancer cells to 5-FU by regulating PI3K/AKT pathways. The inhibition of lncRNA SNHG20 expression could promote the apoptosis and proliferation of 5-FU-resistant colon cancer cells.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>5-Fluorouracil</subject><subject>AKT protein</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Biological activity</subject><subject>Breast cancer</subject><subject>Cadherins - genetics</subject><subject>Cadherins - metabolism</subject><subject>Cancer</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase-3</subject><subject>Cell culture</subject><subject>Cell division</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cell survival</subject><subject>Chemotherapy</subject><subject>Cholecystokinin</subject><subject>Colon</subject><subject>Colon cancer</subject><subject>Colonic Neoplasms - drug therapy</subject><subject>Colonic Neoplasms - genetics</subject><subject>Colonic Neoplasms - pathology</subject><subject>Colorectal cancer</subject><subject>Drug resistance</subject><subject>Drug sensitization</subject><subject>Drug therapy</subject><subject>E-cadherin</subject><subject>Flow cytometry</subject><subject>Fluorouracil - pharmacology</subject><subject>Fluorouracil - therapeutic use</subject><subject>Gastric cancer</subject><subject>Gelatinase B</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Kinases</subject><subject>Matrix metalloproteinase</subject><subject>Matrix Metalloproteinase 9 - metabolism</subject><subject>Matrix metalloproteinases</subject><subject>Medical research</subject><subject>Metalloproteinase</subject><subject>Metastasis</subject><subject>Non-coding RNA</subject><subject>Oncology, Experimental</subject><subject>Ovarian cancer</subject><subject>Phosphatidylinositol 3-Kinases - genetics</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphatidylinositol kinase</subject><subject>Physiological aspects</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Reagents</subject><subject>Reverse transcription</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>RNA, Small Interfering</subject><subject>Survival</subject><subject>Tissue analysis</subject><subject>Tissues</subject><subject>Tumors</subject><subject>Viruses</subject><subject>Western 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of Long Nonencoding Ribonucleic Acid SNHG20 in Colon Cancer Tissue in Its Influences on Chemotherapeutic Sensitivity of Colon Cancer Cells</title><author>Cao, Wenbin ; Zhang, Bo ; Liu, Yang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c476t-faef0813b14d1c6da9747d686a5a441f78e52821c7d00acc7ced86a31f0c3cf83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>5-Fluorouracil</topic><topic>AKT protein</topic><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Biological activity</topic><topic>Breast cancer</topic><topic>Cadherins - genetics</topic><topic>Cadherins - metabolism</topic><topic>Cancer</topic><topic>Caspase 3 - metabolism</topic><topic>Caspase-3</topic><topic>Cell culture</topic><topic>Cell division</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cell survival</topic><topic>Chemotherapy</topic><topic>Cholecystokinin</topic><topic>Colon</topic><topic>Colon cancer</topic><topic>Colonic Neoplasms - drug therapy</topic><topic>Colonic Neoplasms - genetics</topic><topic>Colonic Neoplasms - pathology</topic><topic>Colorectal cancer</topic><topic>Drug resistance</topic><topic>Drug sensitization</topic><topic>Drug therapy</topic><topic>E-cadherin</topic><topic>Flow cytometry</topic><topic>Fluorouracil - pharmacology</topic><topic>Fluorouracil - therapeutic use</topic><topic>Gastric cancer</topic><topic>Gelatinase B</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Kinases</topic><topic>Matrix metalloproteinase</topic><topic>Matrix Metalloproteinase 9 - metabolism</topic><topic>Matrix metalloproteinases</topic><topic>Medical 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Nonencoding Ribonucleic Acid SNHG20 in Colon Cancer Tissue in Its Influences on Chemotherapeutic Sensitivity of Colon Cancer Cells</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2022</date><risdate>2022</risdate><volume>2022</volume><issue>1</issue><spage>4752782</spage><pages>4752782-</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Noncoding RNA (ncRNA) is a kind of RNA that plays a key role in a variety of biological processes, illnesses, and tumours despite the fact that it cannot be translated into proteins. The HT29 colon cancer cell line was utilized to create a 5-FU drug-resistant cell strain (control group), a lentivirus SNHG20 carrier (OE-SNHG20 group), and an SNHG20 shRNA carrier (SNHG20 shRNA carrier group) (SE-SNHG20 group). To determine the expression of cell SNHG20, a real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was utilized, and cholecystokinin-octapeptide (CCK-8) was used to detect the difference in 5-FU inhibitory concentration 50. The goal of the study was to see how variations in long nonencoding ribonucleic acid (lncRNA) SNHG20 expression affect colon cancer cell 5-fluorouracil (5-FU) chemotherapeutic sensitivity by collecting colon cancer and normal para cancer tissues and analysing the differences in SNHG20 expression. The ability of cell cladogenesis was tested using platform cladogenesis. Cell apoptosis was detected using flow cytometry. Western blots revealed the presence of protein phosphatidylinositol kinase (PI3K), protein kinase B (AKT), caspase-3, e-cadherin, and matrix metalloproteinase 9 (MMP-9) enzymes. The findings revealed that SNHG20 expression was considerably upregulated (P<0.05) in colon cancer tissue and 5-FU drug-resistant colon cancer cells. Cell 5-FU IC50, cell cladogenesis, cell survival rate, and MMP-9, P-PI3K, and P-AKT expression were all significantly improved. Cell apoptosis and expressions of E-cadherin and caspase-3, on the other hand, were considerably decreased (P<0.05). Cell 5-FU IC50, cell cladogenesis, cell survival rate, and the expressions of MMP-9, P-PI3K, and P-AKT were all significantly lower in the SE-SNHG20 group, although cell apoptosis and the expressions of E-cadherin and caspase-3 were significantly higher (P<0.05). The results revealed that lncRNA SNHG20 could inhibit the chemotherapeutic sensitivity of colon cancer cells to 5-FU by regulating PI3K/AKT pathways. The inhibition of lncRNA SNHG20 expression could promote the apoptosis and proliferation of 5-FU-resistant colon cancer cells.</abstract><cop>United States</cop><pub>Hindawi</pub><pmid>35915794</pmid><doi>10.1155/2022/4752782</doi><orcidid>https://orcid.org/0000-0001-6364-1241</orcidid><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9338858 |
| source | MEDLINE; PubMed Central Open Access; Wiley Online Library Open Access; PubMed Central; Alma/SFX Local Collection |
| subjects | 1-Phosphatidylinositol 3-kinase 5-Fluorouracil AKT protein Antibodies Apoptosis Apoptosis - genetics Biological activity Breast cancer Cadherins - genetics Cadherins - metabolism Cancer Caspase 3 - metabolism Caspase-3 Cell culture Cell division Cell growth Cell Line, Tumor Cell Proliferation Cell survival Chemotherapy Cholecystokinin Colon Colon cancer Colonic Neoplasms - drug therapy Colonic Neoplasms - genetics Colonic Neoplasms - pathology Colorectal cancer Drug resistance Drug sensitization Drug therapy E-cadherin Flow cytometry Fluorouracil - pharmacology Fluorouracil - therapeutic use Gastric cancer Gelatinase B Gene expression Gene Expression Regulation, Neoplastic Genetic aspects Health aspects Humans Kinases Matrix metalloproteinase Matrix Metalloproteinase 9 - metabolism Matrix metalloproteinases Medical research Metalloproteinase Metastasis Non-coding RNA Oncology, Experimental Ovarian cancer Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism Phosphatidylinositol kinase Physiological aspects Polymerase chain reaction Proteins Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism Reagents Reverse transcription Ribonucleic acid RNA RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism RNA, Small Interfering Survival Tissue analysis Tissues Tumors Viruses Western blotting |
| title | Expression of Long Nonencoding Ribonucleic Acid SNHG20 in Colon Cancer Tissue in Its Influences on Chemotherapeutic Sensitivity of Colon Cancer Cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-24T07%3A46%3A28IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Expression%20of%20Long%20Nonencoding%20Ribonucleic%20Acid%20SNHG20%20in%20Colon%20Cancer%20Tissue%20in%20Its%20Influences%20on%20Chemotherapeutic%20Sensitivity%20of%20Colon%20Cancer%20Cells&rft.jtitle=BioMed%20research%20international&rft.au=Cao,%20Wenbin&rft.date=2022&rft.volume=2022&rft.issue=1&rft.spage=4752782&rft.pages=4752782-&rft.issn=2314-6133&rft.eissn=2314-6141&rft_id=info:doi/10.1155/2022/4752782&rft_dat=%3Cgale_pubme%3EA712138166%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2696736641&rft_id=info:pmid/35915794&rft_galeid=A712138166&rfr_iscdi=true |