Retracted: Effects of FOSL1 silencing on osteosarcoma cell proliferation, invasion and migration through the ERK/AP‐1 signaling pathway

Abstract

Osteosarcoma (OS), as the most frequent primary malignancy of bone, is characterized by the presence of malignant mesenchymal cells. In the current study, our aim was to explore the possible effects Fos-like antigen-1 (FOSL1) had on the silencing regarding OS cell proliferation, invasion, and migration through the activation of the extracellular-signal-regulated kinase (ERK)/activator protein-1 (AP-1) signaling pathway. After the collection of OS on top of already having the adjacent normal tissue samples, the protein positive expression rate of FOSL1 was then measured by implementing the use of immunohistochemistry and discovered that FOSL1 was robustly expressed in OS. Later, to better grasp the impact FOSL1 projects on OS and its underlying mechanism, we determined the OS related genes as well as the ERK/AP-1 signaling pathway related genes expression by using a reversetranscription quantitative polymerase chain reaction and western blot assay techniques. The results of the aforementioned two experiments revealed that the FOSL1 depletion had downregulated the expression of OS related genes by simultaneously downregulating the ERK/AP-1 signaling pathway. Moreover, cell proliferation, cycle, apoptosis, invasion, and migration of FOS1 were all tested by using a cell counting kit-8 assay, flow cytometry, Transwell assay, and scratch test, and these results presented that silencing of the FOSL1 gene inhibited OS cell proliferation, invasion, and migration. Our findings revealed a novel mechanism by which FOSL1 depletion played a significantly negative role in the OS progression through the regulation of the ERK/AP-1 signaling pathway. Functional suppression of FOSL1 might be a future therapeutic strategy regarding OS.

RacGAP1 promotes the malignant progression of cervical cancer by regulating AP-1 via miR-192 and p-JNK

“…AP-1 transcription factor is a dimeric transcription factor encompassing a group of structurally and functionally related members of c-Jun, c-Fos, ATF, and MAF protein families [ 42 – 44 ] and it can therefore form many different combinations of heterodimers and homodimers, and this combination determines the genes that are regulated by AP-1 [ 45 ]. AP-1 can regulate a wide range of biological processes including proliferation, differentiation, apoptosis, survival, migration, invasion, and transformation [ 42 , 44 , 46 – 50 ]. The activation of the AP-1 is regulated at two major levels: extracellular stimuli modulate both the abundance and the activity of AP-1 proteins.…”

Investigating Transcriptional Dynamics Changes and Time-Dependent Marker Gene Expression in the Early Period After Skeletal Muscle Injury in Rats

“…In addition, regarding the 18 network node genes (Figure 5A) that were finally identified in this study, many groups have shown that they play a significant role in the regulation and linkage of related pathways in trauma, skin wound healing, inflammatory processes and inflammation-related diseases, tumor progression, and other inflammation-related biological repair processes (Han et al, 2019;Kumar et al, 2020;Wang et al, 2020) (Table 2). Studies showed that among Fos proteins, including Fosl1, significantly bind to the promoter regions of multiple genes and differentially regulate the expression level of related genes during the processes of tissue and cell damage, repair and differentiation (Reddy and Mossman, 2002).…”

AR-induced long non-coding RNA LINC01503 facilitates proliferation and metastasis via the SFPQ-FOSL1 axis in nasopharyngeal carcinoma

“…Here, SFPQ levels were enriched at the FOSL1 promoter and induced its transcriptional activity in NPC. FOSL1 belongs to the AP-1 transcription factor family and can stimulate tumor cell proliferation and metastasis [ 35 , 36 ]. In this study, FOSL1 promoted NPC cell proliferation, migration and invasion, and ectopic expression of FOSL1 reversed the inhibitory effect of LINC01503 knockdown in NPC.…”