miR‑146a regulates the function of Th17 cell differentiation to modulate cervical cancer cell growth and apoptosis through NF‑κB signaling by targeting TRAF6

Tian, Li; Li, Mengxiong; Xu, Chenyu; Xu, Xiaoyu; Ding, Jie; Cheng, Li; Ou, Rongying

doi:10.3892/or.2019.7046

Cited by 23 publications

(23 citation statements)

References 22 publications

(32 reference statements)

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“…9 miR-146a can alleviate inflammation in psoriasis and can restrain the proliferation of epidermal cells to reduce the infiltration of neutrophils. 10,11 miR-146a is one of the miRNAs expressed most abundantly in the human central nervous system and has been proved to be expressed in a number of nervous system diseases. However, the role of miR-146a in ICH has not yet been specifically studied.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of miR-146a inhibits the apoptosis of hippocampal neurons of rats with cerebral hemorrhage by regulating autophagy

Huan

Jin

et al. 2020

Hum Exp Toxicol

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In this study, to investigate the effect of overexpression of miR-146a on autophagy of hippocampal neurons in rats with intracerebral hemorrhage (ICH), 72 Sprague-Dawley rats were randomly divided into the sham, ICH, miR-146a agomir, and miR-146a agomir control groups. The ICH model was constructed by injection of collagenase VII. The apoptosis of hippocampal neurons was measured by TUNEL assay. The levels of LC3 and Beclin 1 were analyzed by immunohistochemistry. Mitochondrial autophagy was examined by transmission electron microscopy. The levels of LC3A, LC3B, Beclin 1, Bax, Bcl-2, and cleaved caspase 3 were examined by Western blot. Western blot was also used to evaluate the expression of nuclear factor κB signaling pathway-related factors. To examine the effect of autophagy inhibitor (3-methyladenine (3-MA)) on miR-146a-regulated apoptotic protein expression, 30 rats were further divided into the sham, ICH, miR-146a agomir, 3-MA, and miR-146a + 3-MA groups. The levels of Bax, Bcl-2, and cleaved caspase 3 were examined by Western blot. Compared with the sham group, the nerve function scores, brain water content, the percentage of apoptotic cells, and the expression levels of LC3, Beclin 1, Bax, cleaved caspase 3, and p-P65 in the hippocampus of rats in the ICH group were all significantly increased ( p < 0.05), whereas the expression levels of miR-146a, Bcl-2, and p-IκBα were markedly decreased ( p < 0.05). Mitochondrial autophagy was also evident. Furthermore, compared with the ICH group, the results of the abovementioned tests in the miR-146a agomir group were reversed. The overexpression of miR-146a inhibited the autophagy of hippocampal neurons in rats with ICH.

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Section: Introductionmentioning

confidence: 99%

Overexpression of miR-146a inhibits the apoptosis of hippocampal neurons of rats with cerebral hemorrhage by regulating autophagy

Huan

Jin

et al. 2020

Hum Exp Toxicol

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“…microRNA-146a was discovered to upregulate NF-κB by targeting TRAF6 in human cervical cancer (42). In multiple myeloma, TRAF6 was discovered to mediate NF-κB activation and was suggested as a potential therapeutic target (43).…”

Section: Nlrx1 Expression -------------------------------------------mentioning

confidence: 99%

NOD‑like receptor X1, tumor necrosis factor receptor‑associated factor 6 and NF‑κB are associated with clinicopathological characteristics in gastric cancer

Wang

Ye-wei

2021

Exp Ther Med

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Gastric cancer (GC) is a common cancer worldwide and its precise mechanism is largely unknown. The aim of the present study was to evaluate the expression levels of NOD-like receptor X1 (NLRX1), tumor necrosis factor receptor-associated factor 6 (TRAF6) and NF-κB in GC and normal gastric tissue samples to determine the association with the clinicopathological features of GC. GC and adjacent normal gastric tissues from 60 patients with GC were analyzed using immunohistochemistry and western blotting analysis. In addition, the association between NLRX1, TRAF6 and NF-κB expression levels were investigated by Spearman's correlation analysis. The results revealed that NLRX1 protein expression levels were downregulated in the GC tissues compared with the normal gastric tissues (P<0.05). Conversely, TRAF6 and NF-κB protein expression levels were upregulated in the GC tissues compared with the normal gastric tissues (P<0.05). A significant difference was identified between GC patients with high and low expression levels of each protein in the tumor size, vascular invasion, neural invasion, lymph node metastasis, differentiation, gross stage and clinical stage. In addition, a negative correlation was observed between NLRX1 and TRAF6, and NLRX1 and NF-κB expression levels, while a positive correlation was observed between TRAF6 and NF-κB expression levels. In conclusion, NLRX1 expression levels were discovered to be downregulated in GC tissues. The expression levels of NLRX1, TRAF6 and NF-κB were also significantly associated with the clinicopathological characteristics of GC, and the aforementioned results indicated that NLRX1 may be a biomarker in assessing GC.

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“…27 Specifically, Th17 can modulate CC cell growth and apoptosis by the effect of miR-146a or miR155. 28,29 A Th17/Treg imbalance often leads to infection, inflammatory response and autoimmune disorders. 30 Th9 is a newly discovered T cell subset that is suspected to hamper tumor growth in several cancers, and it has been proved that Th9 can inhibit CC progression and immune evasion.…”

Section: Tumor-infiltrating Lymphocyte (Til) T Cellsmentioning

confidence: 99%

<p>Cervical Cancer: Emerging Immune Landscape and Treatment</p>

Guo¹,

Hua²

2020

OTT

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Immune cells are essential for defending the body's balance and have increasingly been implicated in controlling tumor growth. In cervical cancer (CC), the immune landscape is extensively connected with human papillomavirus (HPV) status. Recent insights from studies have revealed that as a result of infection with HPV, immune cell populations such as lymphocytes or monocytes change during carcinogenesis. Immune therapy, in particular checkpoint inhibitors, those targeting PD-1 or PD-L1, has shown promising efficacy. This article reviews the immune landscape and immunotherapy of CC.

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miR‑146a regulates the function of Th17 cell differentiation to modulate cervical cancer cell growth and apoptosis through NF‑κB signaling by targeting TRAF6

Cited by 23 publications

References 22 publications

Overexpression of miR-146a inhibits the apoptosis of hippocampal neurons of rats with cerebral hemorrhage by regulating autophagy

Overexpression of miR-146a inhibits the apoptosis of hippocampal neurons of rats with cerebral hemorrhage by regulating autophagy

NOD‑like receptor X1, tumor necrosis factor receptor‑associated factor 6 and NF‑κB are associated with clinicopathological characteristics in gastric cancer

<p>Cervical Cancer: Emerging Immune Landscape and Treatment</p>

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