2022
DOI: 10.1016/j.canlet.2022.215861
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HULC targets the IGF1R–PI3K-AKT axis in trans to promote breast cancer metastasis and cisplatin resistance

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Cited by 31 publications
(9 citation statements)
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“…As reported previously, long noncoding RNA NBR2 regulated the polarization of tumor-associated macrophages, decreased proliferation, and inhibited migration in colorectal cancer both in vitro and in vivo, which supported our present results. Besides regulation of macrophage polarization, NBR2 was demonstrated to regulate autophagy, suppress migration and invasion, and inhibit epithelial-mesenchymal transition progression in hepatocellular carcinoma, colorectal cancer, osteosarcoma, and nonsmall cell lung cancer, respectively. In addition, recent studies unveiled that many LncRNAs acted as oncogenic or carcinostatic factors in human breast cancer, such as HOTAIR, HULC, SEMA3B-AS1, TGFB2-AS1 etc. We herein provided evidence that LncRNA NBR2 decreased in MWCNTs-stimulated macrophages, participating in macrophage M2 polarization and consequently promoted metastasis of breast cancer cells. However, the exact mechanism of the downregulation of NBR2 induced by MWCNT exposure in macrophages still needs to be further explored.…”
Section: Discussionmentioning
confidence: 71%
“…As reported previously, long noncoding RNA NBR2 regulated the polarization of tumor-associated macrophages, decreased proliferation, and inhibited migration in colorectal cancer both in vitro and in vivo, which supported our present results. Besides regulation of macrophage polarization, NBR2 was demonstrated to regulate autophagy, suppress migration and invasion, and inhibit epithelial-mesenchymal transition progression in hepatocellular carcinoma, colorectal cancer, osteosarcoma, and nonsmall cell lung cancer, respectively. In addition, recent studies unveiled that many LncRNAs acted as oncogenic or carcinostatic factors in human breast cancer, such as HOTAIR, HULC, SEMA3B-AS1, TGFB2-AS1 etc. We herein provided evidence that LncRNA NBR2 decreased in MWCNTs-stimulated macrophages, participating in macrophage M2 polarization and consequently promoted metastasis of breast cancer cells. However, the exact mechanism of the downregulation of NBR2 induced by MWCNT exposure in macrophages still needs to be further explored.…”
Section: Discussionmentioning
confidence: 71%
“…Besides, except PIK3CA and AKT, we also found IGF1R, MAPK1, JAK3, STAT5A and ESR1 have a relatively higher binding affinity with LEO components. IGF1R is a trans -membrane tyrosine kinase receptor and frequently up-regulated in breast cancer [ 27 ]. The interaction between the molecules IGF-I and IGF-II, along with the receptor IGF1R, triggers powerful signals that promote cell growth and prevent cell death via the pathways PI3K/AKT and RAS/MAPK [ 28 ].…”
Section: Discussionmentioning
confidence: 99%
“…Zhou et al. demonstrated that lncRNA HULC can increase H3K9 acetylation in the promoter region of IGF1R in the nucleus, thereby activating IGF1R transcription, which in turn causes activation of the downstream PI3K/AKT pathway ( 121 ). DLEU1 is highly expressed in breast cancer and is subject to two epigenetic modifications to regulate its expression.…”
Section: Interactions Between Ncrnas and Other Epigenetic Modificatio...mentioning
confidence: 99%