Exploration of the regulatory mechanism of norcantharidin on sine oculis homeobox homolog 4 in colon cancer using transcriptome sequencing and bioinformatic
Objective: To explore the key molecules regulated by norcantharidin (NCTD) in colon cancer treatment. Methods: We used cell counting kit-8 and 5-ethnyl-2′-deoxyuridine/Hoechst staining assays to study the effects of NCTD on cell proliferation in colon cancer. Annexin V-fluorescein isothiocyanate/pro...
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Elsevier
2025-04-01
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| Series: | Journal of Traditional Chinese Medical Sciences |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2095754825000109 |
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| author | Fanqin Zhang Chao Wu Jingyuan Zhang Zhihong Huang Antony Stalin Yiyan Zhai Shuqi Liu Jiarui Wu |
| author_facet | Fanqin Zhang Chao Wu Jingyuan Zhang Zhihong Huang Antony Stalin Yiyan Zhai Shuqi Liu Jiarui Wu |
| author_sort | Fanqin Zhang |
| collection | DOAJ |
| description | Objective: To explore the key molecules regulated by norcantharidin (NCTD) in colon cancer treatment. Methods: We used cell counting kit-8 and 5-ethnyl-2′-deoxyuridine/Hoechst staining assays to study the effects of NCTD on cell proliferation in colon cancer. Annexin V-fluorescein isothiocyanate/propidium iodide staining was used to evaluate apoptosis, whereas Transwell assays were conducted to evaluate migration and invasion. We performed RNA sequencing to analyze the changes in gene expression after treatment. Differential analysis was performed using differential expression sequencing 2 (Deseq2) in R. Cytoscape was used to construct a competing endogenous RNA (ceRNA) network and Gene Expression Omnibus (GEO) datasets were used to validate sine oculis homeobox homolog 4 (SIX4) expression in colon cancer tissues. Furthermore, the prognostic potential of SIX4 was evaluated using receiver-operating characteristic curves. We conducted an immune infiltration analysis to explore the SIX4 relationship with the immune microenvironment in colon cancer. Finally, SIX4 expression, pan-cancer prognosis, tumor mutation burden (TMB) correlations, microsatellite instability (MSI), and mismatch repair (MMR) were analyzed. Results: NCTD inhibited colon cancer cell proliferation (P < .0001), induced apoptosis (P = .0007), and suppressed the migration and invasion of colon cancer cells. The H19/miR-193b-3p/SIX4 axis was identified as the key ceRNA network involved in the anticancer activity of NCTD. SIX4 is highly expressed in colon cancer tissues, shortening patient survival and affecting immune infiltration. A pan-cancer analysis showed that SIX4 overexpression affects the survival of various cancers. Finally, we correlated SIX4 expression with TMB, MSI, and MMR expression. Conclusion: NCTD inhibits the malignant behaviour of colon cancer cells. SIX4 is abnormally expressed in multiple tumor types, significantly affecting the overall survival of patients with cancer, and is a core regulatory target of NCTD in the treatment of colon cancer. |
| format | Article |
| id | doaj-art-a59bcf7416d64dcbacb0c52435f4bb43 |
| institution | Kabale University |
| issn | 2095-7548 |
| language | English |
| publishDate | 2025-04-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of Traditional Chinese Medical Sciences |
| spelling | doaj-art-a59bcf7416d64dcbacb0c52435f4bb432025-08-20T03:53:27ZengElsevierJournal of Traditional Chinese Medical Sciences2095-75482025-04-0112225927610.1016/j.jtcms.2025.03.006Exploration of the regulatory mechanism of norcantharidin on sine oculis homeobox homolog 4 in colon cancer using transcriptome sequencing and bioinformaticFanqin Zhang0Chao Wu1Jingyuan Zhang2Zhihong Huang3Antony Stalin4Yiyan Zhai5Shuqi Liu6Jiarui Wu7School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 102488, ChinaSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 102488, ChinaSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 102488, ChinaSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 102488, ChinaXavier Research Foundation, St Xavier's College, Affiliated to Manonmaniam Sundaranar University, Palayamkottai 627002, IndiaSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 102488, ChinaSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 102488, ChinaSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 102488, China; Corresponding author.Objective: To explore the key molecules regulated by norcantharidin (NCTD) in colon cancer treatment. Methods: We used cell counting kit-8 and 5-ethnyl-2′-deoxyuridine/Hoechst staining assays to study the effects of NCTD on cell proliferation in colon cancer. Annexin V-fluorescein isothiocyanate/propidium iodide staining was used to evaluate apoptosis, whereas Transwell assays were conducted to evaluate migration and invasion. We performed RNA sequencing to analyze the changes in gene expression after treatment. Differential analysis was performed using differential expression sequencing 2 (Deseq2) in R. Cytoscape was used to construct a competing endogenous RNA (ceRNA) network and Gene Expression Omnibus (GEO) datasets were used to validate sine oculis homeobox homolog 4 (SIX4) expression in colon cancer tissues. Furthermore, the prognostic potential of SIX4 was evaluated using receiver-operating characteristic curves. We conducted an immune infiltration analysis to explore the SIX4 relationship with the immune microenvironment in colon cancer. Finally, SIX4 expression, pan-cancer prognosis, tumor mutation burden (TMB) correlations, microsatellite instability (MSI), and mismatch repair (MMR) were analyzed. Results: NCTD inhibited colon cancer cell proliferation (P < .0001), induced apoptosis (P = .0007), and suppressed the migration and invasion of colon cancer cells. The H19/miR-193b-3p/SIX4 axis was identified as the key ceRNA network involved in the anticancer activity of NCTD. SIX4 is highly expressed in colon cancer tissues, shortening patient survival and affecting immune infiltration. A pan-cancer analysis showed that SIX4 overexpression affects the survival of various cancers. Finally, we correlated SIX4 expression with TMB, MSI, and MMR expression. Conclusion: NCTD inhibits the malignant behaviour of colon cancer cells. SIX4 is abnormally expressed in multiple tumor types, significantly affecting the overall survival of patients with cancer, and is a core regulatory target of NCTD in the treatment of colon cancer.http://www.sciencedirect.com/science/article/pii/S2095754825000109Colon cancerNorcantharidinSIX4BioinformaticsPan-cancer |
| spellingShingle | Fanqin Zhang Chao Wu Jingyuan Zhang Zhihong Huang Antony Stalin Yiyan Zhai Shuqi Liu Jiarui Wu Exploration of the regulatory mechanism of norcantharidin on sine oculis homeobox homolog 4 in colon cancer using transcriptome sequencing and bioinformatic Journal of Traditional Chinese Medical Sciences Colon cancer Norcantharidin SIX4 Bioinformatics Pan-cancer |
| title | Exploration of the regulatory mechanism of norcantharidin on sine oculis homeobox homolog 4 in colon cancer using transcriptome sequencing and bioinformatic |
| title_full | Exploration of the regulatory mechanism of norcantharidin on sine oculis homeobox homolog 4 in colon cancer using transcriptome sequencing and bioinformatic |
| title_fullStr | Exploration of the regulatory mechanism of norcantharidin on sine oculis homeobox homolog 4 in colon cancer using transcriptome sequencing and bioinformatic |
| title_full_unstemmed | Exploration of the regulatory mechanism of norcantharidin on sine oculis homeobox homolog 4 in colon cancer using transcriptome sequencing and bioinformatic |
| title_short | Exploration of the regulatory mechanism of norcantharidin on sine oculis homeobox homolog 4 in colon cancer using transcriptome sequencing and bioinformatic |
| title_sort | exploration of the regulatory mechanism of norcantharidin on sine oculis homeobox homolog 4 in colon cancer using transcriptome sequencing and bioinformatic |
| topic | Colon cancer Norcantharidin SIX4 Bioinformatics Pan-cancer |
| url | http://www.sciencedirect.com/science/article/pii/S2095754825000109 |
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