TAB3 promotes human esophageal squamous cell carcinoma proliferation and invasion via the NF‑κB pathway

Abstract

Esophageal squamous cell carcinoma (ESCC) has become one of the most common causes of cancer‑associated mortality worldwide. Transforming growth factor‑activated kinase (TAK1)‑binding protein 3 (TAB3) is essential for activation of the NF (NF)‑κB pathway in response to TAK1 activation. The NF‑κB pathway serves important roles in tumor cell proliferation and migration; however, the clinical relevance of TAB3 and its biological function in ESCC progression remain elusive. The present study investigated the expression and function of TAB3 in ESCC tissues, and its association with the clinical prognosis of patients. The results demonstrated that TAB3 expression was significantly increased in human ESCC cell lines and tissue samples, and the expression of TAB3 was associated with ESCC lymph node metastasis, T stage, pathological grade and Ki‑67 expression in 80 ESCC samples, as determined by immunohistochemistry. Patients with ESCC and high TAB3 expression exhibited worse overall survival. Furthermore, knockdown of TAB3 by small interfering RNA inhibited the proliferation of ESCC cells, and reduced the migration and invasion of ESCC cells. In addition, knockdown of TAB3 decreased the expression of the NF‑κB pathway in TE‑1 cells. Taken together, these results demonstrated that TAB3 may be a promising therapeutic target for the treatment of ESCC.

ZFPM2-AS1 facilitates cell growth in esophageal squamous cell carcinoma via up-regulating TRAF4

“…NF-κB is a significant contributor to initiation and progression of various cancers via controlling tumor cell proliferation, survival, migration, inflammation, invasion and angiogenesis [32]. Also, NF-κB pathway was reported to facilitate ESCC cell proliferation and invasion [33]. The previous studies have pointed out that TRAF4 could activate NF-κB to accelerate cancer development [34,35].…”

Hsa-microRNA-27b-3p inhibits hepatocellular carcinoma progression by inactivating transforming growth factor-activated kinase-binding protein 3/nuclear factor kappa B signalling

“…Multiple researchers have documented that the NF-кB signalling pathway is constitutively activated and may act as a promising target for the treatment of HCC [23,44]. TAB3 is involved in regulating differentiation and progression in several cancer types by modulating NF-кB signalling [27,29,30,45]. In HCC, hsa-miR-195 suppressed cell proliferation and migration in vitro and in vivo by decreasing the expression of multiple NF-κB downstream effectors via direct targeting of IKKα and TAB3 [46].…”

“…Upon certain cell stimulation, such as tumour necrosis factor alpha (TNF-α), interleukin-1 and lipopolysaccharide, the activated IκB kinase (IKK) complex induces the phosphorylation and degradation of IκB proteins, which subsequently liberates NF-κB to the nucleus and initiates transcriptional processes [19,25]. TAB3 is dysregulated in a variety of cancers [26][27][28] and participates in the activation of the NF-кB pathway [29,30]. Alfredo Criollo et al reported that overexpression of TAB3 suppressed, while depletion of TAB3 triggered, autophagy in HeLa cells [31].…”

The oncogene EIF3c promotes esophageal squamous cell carcinoma tumorigenesis by inhibiting cell proliferation and inducing cell apoptosis

“…MAPK/ERK signaling pathway was involved in the proliferation inhibition induced by miR-148a/MAP3K9 axis in ESCC cells [32]. NF-κB signaling was reported as the downstream target pathway in regulation of proliferation and apoptosis in ESCC cells by several gene, such as transforming growth factoractivated kinase (TAK1)binding protein 3 (TAB3) and NKILA (a long non-coding RNA) [33,34]. Our previous study also showed that death receptor signaling mediated by ROS-DR5 axis taken part in the induction of apoptosis by Isoalantolactone in ESCC cell.…”