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<article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="research-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Combinatorial Chemistry &amp; High Throughput Screening</journal-id><journal-title-group><journal-title xml:lang="en">Combinatorial Chemistry &amp; High Throughput Screening</journal-title><trans-title-group xml:lang="ru"><trans-title>Combinatorial Chemistry &amp; High Throughput Screening</trans-title></trans-title-group></journal-title-group><issn publication-format="print">1386-2073</issn><issn publication-format="electronic">1875-5402</issn><publisher><publisher-name xml:lang="en">Bentham Science</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">643731</article-id><article-id pub-id-type="doi">10.2174/1386207326666230504144758</article-id><article-categories><subj-group subj-group-type="toc-heading"><subject>Chemistry</subject></subj-group><subj-group subj-group-type="article-type"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">miR-141-3p Enhanced Radiosensitivity of CRC Cells</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Peng</surname><given-names>Lizhong</given-names></name><email>info@benthamscience.net</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name><surname>Li</surname><given-names>Pan</given-names></name><email>info@benthamscience.net</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name><surname>Peng</surname><given-names>Zexu</given-names></name><email>info@benthamscience.net</email><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff id="aff1"><institution>Department of Surgery, Hubei Hospital of Chinese Medicine</institution></aff><pub-date date-type="pub" iso-8601-date="2024-01-01" publication-format="electronic"><day>01</day><month>01</month><year>2024</year></pub-date><volume>27</volume><issue>1</issue><fpage>118</fpage><lpage>126</lpage><history><date date-type="received" iso-8601-date="2025-01-07"><day>07</day><month>01</month><year>2025</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2024, Bentham Science Publishers</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="en">Bentham Science Publishers</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/></permissions><self-uri xlink:href="https://journals.eco-vector.com/1386-2073/article/view/643731">https://journals.eco-vector.com/1386-2073/article/view/643731</self-uri><abstract xml:lang="en"><p id="idm46041443791696">Background:Colorectal cancer (CRC) is recognized as one of the frequently diagnosed malignancies, and numerous microRNAs (miRs) are identified to be active in CRC.</p><p id="idm46041443795696">Objective:This work aimed to clarify the effect of miR-141-3p on the radiosensitivity of CRC cells.</p><p id="idm46041443799664">Methods:Firstly, CRC cell lines were cultured and applied to construct radiation-resistant CRC cells via X-ray treatment. The expression levels of miR-141-3p and long non-coding RNA DLX6 antisense RNA 1 (lncRNA DLX6-AS1) in CRC cells were measured using real-time quantitative polymerase chain reaction. After transfection with miR-141-3p mimics and 24 h treatment with 6- MV X-ray (0, 2, 4, 6 Gy), the survival fraction (SF) and the colony formation ability of CRC cells were determined using the cell counting kit-8 and colony formation methods. The interactions between miR-141-3p and DLX6-AS1 were analyzed using the dual-luciferase assay. The impact of miR-141-3p on DLX6-AS1 stability was detected after adding actinomycin-D. The role of DLX6- AS1 in the radiosensitivity of CRC cells was explored by transfecting oe-DLX6-AS1 into radiation- resistant CRC cells overexpressing miR-141-3p.</p><p id="idm46041443804720">Results:The relative expression levels of miR-141-3p were downregulated in CRC cells and further declined in radiation-resistant cells. Upregulation of miR-141-3p relative expression reduced SF and the colony formation ability while amplifying the radiosensitivity of radiation-resistant CRC cells. miR-141-3p directly bound to DLX6-AS1 to reduce DLX6-AS1 stability, and therefore downregulated DLX6-AS1 expression. DLX6-AS1 overexpression counteracted the role of miR- 141-3p overexpression in amplifying the radiosensitivity of radiation-resistant CRC cells.</p><p id="idm46041443814096">Conclusion:miR-141-3p binding to DLX6-AS1 significantly decreased DLX6-AS1 stability and expression, promoting the radiosensitivity of CRC cells.</p></abstract><kwd-group xml:lang="en"><kwd>Colorectal cancer</kwd><kwd>miR-141-3p</kwd><kwd>lncRNA DLX6-AS1</kwd><kwd>radiotherapy</kwd><kwd>radiosensitivity</kwd><kwd>RNA stability</kwd><kwd>colon cancer</kwd><kwd>rectal cancer.</kwd></kwd-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Lichtenstern, C.R.; Ngu, R.K.; Shalapour, S.; Karin, M. Immunotherapy, inflammation and colorectal cancer. Cells, 2020, 9(3), 618. doi: 10.3390/cells9030618 PMID: 32143413</mixed-citation></ref><ref id="B2"><label>2.</label><mixed-citation>Dekker, E.; Tanis, P.J.; Vleugels, J.L.A.; Kasi, P.M.; Wallace, M.B. Colorectal cancer. 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