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Interleukin-6 and hepatocyte growth factor produce from chromosomal aberrant cholangiocarcinoma-associated fibroblasts |
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| รหัสดีโอไอ | |
| Creator | Suyanee Thongchot, Penkhae Utaijaratrasmi, Pranisa Jamjantra, Worapa Heepchantree, Kulthida Vaeteewoottacharn, Sopit Wongkham, Peti Thuwajit, Chanitra Thuwajit |
| Title | Interleukin-6 and hepatocyte growth factor produce from chromosomal aberrant cholangiocarcinoma-associated fibroblasts |
| Contributor | Suyanee Thongchot, Penkhae Utaijaratrasmi, Pranisa Jamjantra, Worapa Heepchantree, Kulthida Vaeteewoottacharn, Sopit Wongkham, Peti Thuwajit, Chanitra Thuwajit |
| Publisher | Genetics Society of Thailand |
| Publication Year | 2563 |
| Journal Title | Genomics and Genetics |
| Journal Vol. | 13 |
| Journal No. | 2&3 |
| Page no. | 33-43 |
| Keyword | fibroblast, cholangiocarcinoma, migration, chromosomal aberration, interleukin-6 |
| URL Website | https://li01.tci-thaijo.org/index.php/gst/issue/view/16872 |
| Website title | https://li01.tci-thaijo.org/index.php/gst/article/view/244292 |
| ISSN | 24655198 |
| Abstract | Cholangiocarcinoma (CCA)-associated fibroblasts(CCFs) have been identified as thecancer progression impact through the aberrant production of tumorigenic substances. This study is aimed to investigate the production of tumor-related cytokines from primary culture CCFs andtheir tumorigenic properties in context of CCA. Primary culture CCFs were isolated from fresh CCA tissuesand verified by morphology, chromosomal pattern, and the expressions of fibroblast markers: vimentin (VIM), alpha-smooth muscle actin (ASMA); epithelial markers: cytokeratin 7 and 19 (CK7 and CK19); and periostin (PN). Migration induction of the conditioned-media (CM) from CCFs on CCA cells was shown by wound healing assay. The results revealed that all CCFs had the spindle-liked morphologies and the presence of VIM, ASMA and PN, but notCK19. Additionally, CCFs-CM induced migration of CCA cells. CCFs had aberrant chromosomal patternsincluding tetraploid and diploid chromosomeswith deletion, amplification and translocation. The abnormal karyotypes were 92,XXYY; 46,X,-Y,+7; 46,XY,der(8)t(8;?); 92,XXYY,der(8)t(8;?),der(8)t(8;?);and 92,XX,-Y,-Y,+7,+7.In contrast, normal skin fibroblasts (NLFs) exhibited diploid chromosome with50% had Y-chromosome deletion. Furthermore,upregulationsof hepatocyte growth factor (HGF) and interleukin-6 (IL-6) with increasedrecruitment of CCF-CMs wereobserved.IL-6and hepatocyte growth factor located on chromosome 7 showed increased expressionsand IL-6 was confirmed the increment in more CCF-CMs.These observations provide the evidencesthat dysregulation of IL-6,a tumorigenic substancefrom CCFs,may be resultedfrom chromosomal aberrations. These data give us an experimental foundation for further studies to explore the mechanism underliningthe involvement of fibroblasts in CCA progression. |
