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Toxic Effects and Biodistribution of Ultrasmall Gold Nanoparticles *
Published in Valerio Voliani, Nanomaterials and Neoplasms, 2021
Gunter Schmid, Wolfgang G. Kreyling, Ulrich Simon
Following the initial growth response, heat shock and stress-related genes were upregulated after 6 h and strongly upregulated after 12 h in Au1.4MS-treated but not in Au15MS-treated or untreated HeLa cells. This group of genes (HSPA1A, DNAJA4, CHAC1, HSPA1A, DDIT3, GEM, LOC387763, PGF, HSPA6, SESN2, LOC284561, PPP1R15A, HMOX1, C16orf81, LOC344887, NGF, OSGIN1, FOSL1, CXCL2, IL8) suggested that a robust stress response had occurred in the Au1.4MS-treated cells. Highly elevated expression of heat shock proteins has been demonstrated to inhibit apoptosis at several stages including blocking of cytochrome c release from mitochondria, thus preventing the formation of an apoptosome and the activation of caspase-3, ultimately forcing cells into necrosis instead of apoptosis.
The molecular mechanisms and targeting strategies of transcription factors in cholangiocarcinoma
Published in Expert Opinion on Therapeutic Targets, 2022
Jiao Wang, Fujing Ge, Tao Yuan, Meijia Qian, Fangjie Yan, Bo Yang, Qiaojun He, Hong Zhu
The transcription factor Fos-related antigen 1 (FOSL1), a member of the AP1 complex, heterodimerizes with JUNs to promote transcription and plays an important role in cell differentiation and tumorigenesis [12]. A study analyzes and builds the transcriptional regulatory network in CCA and finds that FOSL1 may be a key transcription factor affecting the progression of CCA [47]. One study finds that the protein expression of FOSL1 is upregulated in CCA and correlates with poor survival. FOSL1 directly binds the promoter of HMGCS1 to control its expression and promotes cell proliferation and cell cycle progression in CCA cells [8,12]. Surprisingly, high FOSL1 expression is associated with KRAS mutations, and patients with tumors carrying both KRAS mutations and high FOSL1 expression tended to have the worst survival [8]. Another study shows that FOSL1 as a downstream target gene of TCF7 is required for TCF7-induced PHCC proliferation [48].
A comprehensive analysis of Wnt/β-catenin signaling pathway-related genes and crosstalk pathways in the treatment of As2O3 in renal cancer
Published in Renal Failure, 2018
Yan-Lei Li, Yu-Fen Jin, Xiu-Xia Liu, Hong-Jun Li
FOSL1 encodes fos-like antigen 1, also known as Fra1, a member of Fos gene family, which regulates cell proliferation, differentiation, and transformation [30]. FOSL1 can function as either an activator or a repressor to control the equilibrium between migration and adhesion in sprouting angiogenesis, which is critical in tumorigenesis [31,32]. In this study, FOSL1 was up-regulated in the 786-O cells with As2O3 treatment, while a study has reported that Fosl1 induces transformation and invasiveness of human epithelial adenocarcinoma cells [33], which is inconsistent with the result of this study. It may be due to that during the early stage of As2O3 treatment, the expression of FOSL1 is not effectively influenced, and with the prolonged time of As2O3 treatment, the expression of FOSL1 may be decreased, which is needed to be further investigated.
Low expression of FOSL1 is associated with favorable prognosis and sensitivity to radiation/pharmaceutical therapy in lower grade glioma
Published in Neurological Research, 2020
Jin Zhu, Ya-Peng Zhao, Yu-Qi Zhang
FOSL1, as an important transcription factor, participates in numerous biological processes. It can contribute significantly to bone development [19], somatic cell reprogramming processes [20], and embryonic development [8]. FOSL1 is overexpressed in various cancers such as breast cancer [13], lung cancer [9], and hepatocellular carcinoma [21]. Although some research has shown that FOSL1 has a prominent role in the tumorigenicity of malignant glioma cells [14,15], little is known about its function in LGG.