RETRACTED: Luteolin retards CXCL12-induced Jurkat cells migration by disrupting transcription of CXCR4

Bu, Yunwen; Zhao, Dandan

doi:10.1016/j.yexmp.2020.104370

Cited by 3 publications

(2 citation statements)

References 34 publications

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“…Chemokines secreted by tumor cells involve the recruitment of monocytes, such as CCL2, CCL5, and CXCL12 (Mantovani et al, 2017). Colon cancer cells with high expression of CXCL12 recruit macrophages to form the angiogenesis niches for supporting revascularization of tumor growth (Bu & Zhao, 2020; Rigo et al, 2010). We found triptolide treatment suppressed the expression of CXCL12 in CT26 and HT29 cell lines.…”

Section: Discussionmentioning

confidence: 99%

Triptolide decreases tumor‐associated macrophages infiltration and M2 polarization to remodel colon cancer immune microenvironment via inhibiting tumor‐derived CXCL12

Jiang

Cao²,

Gao

et al. 2020

Journal Cellular Physiology

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Colon cancer is a common and deadly human digestive tract malignant tumor with poor prognosis. Immunotherapy has elicited tremendous success as a treatment modality for multiple solid tumors. Triptolide is extracted from the traditional Chinese medicine Tripterygium wilfordii Hook. F which shows various pharmacological actions including antitumor, anti-inflammatory, antimicrobial, antifibrosis, and antirheumatic. However, the influence of triptolide treatment on remodeling tumor immune microenvironment is still unknown in colon cancer. This study was aimed to investigate the therapeutic effect of triptolide treatment on colon cancer and the impact on tumor immune microenvironment and its underlying mechanism. We used CT26 subcutaneous tumors to conduct in vivo experiments and HT29, CT16, and Raw264.7 cells to perform in vitro assays. Triptolide had a therapeutic effect against colon cancer in vivo. Triptolide treatment distinctly inhibited the proliferation of colon cancer cells and induced apoptosis in vitro. In colon cancer immune microenvironment, triptolide treatment decreased the infiltration of tumor-associated macrophages through downregulating tumor-derived CXCL12 expression via nuclear factor kappa B and extracellular signal-regulated protein kinases 1 and 2 axis to remodel the immune microenvironment. Triptolide-educated colon cancers retarded the macrophages polarize to anti-inflammatory M2 status by decreasing the expression of Arg-1, CD206, and interleukin-10. Moreover, triptolide inhibited the migration of colon cancer cells via decreasing vascular endothelial growth factor expression. Our results identified the role of triptolide treatment in remodeling colon cancer immune microenvironment along with the distinct cytotoxicity function against colon cancer cells, which may provide the evidence for triptolide treatment in clinical.

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Section: Discussionmentioning

confidence: 99%

Triptolide decreases tumor‐associated macrophages infiltration and M2 polarization to remodel colon cancer immune microenvironment via inhibiting tumor‐derived CXCL12

Jiang

Cao²,

Gao

et al. 2020

Journal Cellular Physiology

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“…MMP-9, as an indicator of migration, has been reported to be a downstream target of CXCL12/CXCR4 (Zuo et al, 2017). Thus, curcumin and luteolin impair the migratory activity in tumor cells by the repression of the CXCL12/CXCR4 biological axis, as a consequence of the downregulation of MMP-9 by luteolin (Qin et al, 2018;Bu and Zhao, 2020). Our results imply that rP21 repressed CXCL12-induced migration and invasion and decreased MMP-9 expression.…”

Section: Discussionmentioning

confidence: 52%

The Recombinant Protein Based on Trypanosoma cruzi P21 Interacts With CXCR4 Receptor and Abrogates the Invasive Phenotype of Human Breast Cancer Cells

Borges

Uehara

Santos

et al. 2020

Front. Cell Dev. Biol.

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Trypanosoma cruzi P21 is a protein secreted by the parasite that plays biological roles directly involved in the progression of Chagas disease. The recombinant protein (rP21) demonstrates biological properties, such as binding to CXCR4 receptors in macrophages, chemotactic activity of immune cells, and inhibiting angiogenesis. This study aimed to verify the effects of rP21 interaction with CXCR4 from non-tumoral cells (MCF-10A) and triple-negative breast cancer cells (MDA-MB-231). Our data showed that the MDA-MB-231 cells expressed higher levels of CXCR4 than did the non-tumor cell lines. Besides, cytotoxicity assays using different concentrations of rP21 showed that the recombinant protein was non-toxic and was able to bind to the cell membranes of both cell lineages. In addition, rP21 reduced the migration and invasion of MDA-MB-231 cells by the downregulation of MMP-9 gene expression. In addition, treatment with rP21 blocked the cell cycle, arresting it in the G1 phase, mainly in MDA-MB-231 cells. Finally, rP21 prevents the chemotaxis and proliferation induced by CXCL12. Our data showed that rP21 binds to the CXCR4 receptors in both cells, downregulates CXCR4 gene expression, and decreases the receptors in the cytoplasm of MDA-MB-231 cells, suggesting CXCR4 internalization. This internalization may explain the desensitization of the receptors in these cells. Thus, rP21 prevents migration, invasion, and progression in MDA-MB-231 cells.

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Retrakcje w filozofii na podstawie bazy Retraction Watch w świetle wytycznych Komisji Etyki Publikacji

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Łyszczarz

2022

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Artykuł prezentuje wyniki analizy ilościowej i jakościowej zawiadomień o retrakcji w publikacjach z zakresu filozofii (o zasięgu globalnym) zawartych w Retraction Watch Database, z punktu widzenia zaleceń Komisji Etyki Publikacji. Pod względem ilościowym próba wynosi jedynie 0,48% rekordów w całej bazie, przez co trudno uznać ją za reprezentatywną dla dyscypliny, a tym bardziej niemożliwe jest uogólnienia wniosków na całą aktywność naukową. Statystyka wycofań publikacji może być jednak podstawą do studium przypadków. Treść zawiadomień jest często niekompletna lub niejednoznaczna. Normatywne uregulowania retrakcji publikacji w odniesieniu do przedmiotu badań należy uznać za nie w pełni adekwatne do specyfiki praktyki wydawniczej w filozofii.

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RETRACTED: Luteolin retards CXCL12-induced Jurkat cells migration by disrupting transcription of CXCR4

Cited by 3 publications

References 34 publications

Triptolide decreases tumor‐associated macrophages infiltration and M2 polarization to remodel colon cancer immune microenvironment via inhibiting tumor‐derived CXCL12

Triptolide decreases tumor‐associated macrophages infiltration and M2 polarization to remodel colon cancer immune microenvironment via inhibiting tumor‐derived CXCL12

The Recombinant Protein Based on Trypanosoma cruzi P21 Interacts With CXCR4 Receptor and Abrogates the Invasive Phenotype of Human Breast Cancer Cells

Retrakcje w filozofii na podstawie bazy Retraction Watch w świetle wytycznych Komisji Etyki Publikacji

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