The Role of Tumor Necrosis Factor α in the Biology of Uterine Fibroids and the Related Symptoms

Ciebiera, Michał; Włodarczyk, Marta; Zgliczyńska, Magdalena; Łukaszuk, Krzysztof; Męczekalski, Błażej; Kobierzycki, Christopher; Łoziński, Tomasz; Jakiel, Grzegorz

doi:10.3390/ijms19123869

Cited by 58 publications

(56 citation statements)

References 206 publications

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“…Furthermore, TNFα is a cytokine that is responsible for inhibiting endometrial proliferation and induces apoptosis. Previous studies have shown that endometrial cells produce increased concentration of TNFα during menstruation [35]. Moreover, Dogru et al showed that the TNF -308G > A gene polymorphism is strongly associated with susceptibility to dysmenorrhea in the Turkish female population [36].…”

Section: Tumour Necrosis Factors Alpha (Tnfα)mentioning

confidence: 99%

Inflammatory Markers in Dysmenorrhea and Therapeutic Options

Barcikowska

Rajkowska-Labon

Grzybowska

et al. 2020

IJERPH

138

115

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Dysmenorrhea often significantly reduces the quality of women’s life and is still an important public health problem. Despite numerous studies, the pathomechanism of dysmenorrhea is not fully understood. Previous research indicates the complexity of biochemical reactions between the endocrine, vascular, and immune systems. Prostaglandins play a major role in the pathomechanism of dysmenorrhea. In contrast, cytokines and other proinflammatory factors in primary dysmenorrhea are less studied. In addition to the applied pharmacotherapy, more and more studies proving the effectiveness of non-pharmacological methods appear. Therefore, the present work contains a review of the latest research concerning factors involved in dysmenorrhea, as well as therapeutic options. In the literature search, authors used online databases, PubMed, and clinitrials.gov and browsed through individual gynecology, physiotherapy journals and books.

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Section: Tumour Necrosis Factors Alpha (Tnfα)mentioning

confidence: 99%

Inflammatory Markers in Dysmenorrhea and Therapeutic Options

Barcikowska

Rajkowska-Labon

Grzybowska

et al. 2020

IJERPH

138

115

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“…To investigate the role of THRIL in the OS development, the xenograft model of human MG63 cells was established, MG63 cells were transfected with lentivirus vector of siRNA-THRIL, or negative control, 2×10 6 conditional MG63 cells were subcutaneously injected in rear flank of nude mice (6 per group), TNF-α (500 ng/mice) was treated i.p. twice a week for 3 weeks.…”

Section: Tumor Modelmentioning

confidence: 99%

“…5 Accumulating evidence indicated that, in addition to being produced by immune cells within the tumor-associated microenvironment, TNFα can be produced by a wide variety of malignant cells, including OS cells. 6 Li et al reported that TNF-α may enhance the adaptive immune resistance mediated by IFN-γ-induced B7-H1 in hepatocellular carcinoma cells. 7 TNF-α expression in ovarian carcinoma varies by histologic subtype and provides some support for the role of inflammation in ovarian carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

<p>Upregulated lncRNA THRIL/TNF-α Signals Promote Cell Growth and Predict Poor Clinical Outcomes of Osteosarcoma</p>

Xu¹,

Jin²,

Yang³

et al. 2020

OTT

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Background: The immunosuppressive facet and tumorigenic role of TNF-α have been revealed in osteosarcoma (OS). Long noncoding RNA THRIL is identified to regulate TNF-α expression and participates in immune response. Thus, investigations on the clinical expression pattern of THRIL/TNF-α signal in OS would provide a potential target premise for OS patients. Methods: We collected OS (n=83), nontumor tissues (n=37) and serum samples (n=83 for OS and n=40 for healthy control) to determine the expressions and clinical significance of THRIL/TNF-α signal. Knockdown of THRIL in OS cell lines MG63 and Saos2 in vitro and in vivo was performed to confirm its function in the development of OS. Results: Elevated expression of THRIL was associated with increased TNF-α levels in OS tissues and serum samples. Combination of THRIL and TNF-α in tissues showed a more efficient diagnostic value for OS patients than either of them. Moreover, high-expressed THRIL was associated with larger tumor size, advanced Enneking stage and lung metastasis, whereas high TNF-α expression was found in patients with high histologic grade and patients who simultaneously harbor high THRIL and TNF-α showed the worst overall survival and metastasis-free survival. TNF-α signals increased OS cell vitalities in vitro but knockdown of THRIL inhibited TNF-α expressions, leading to impaired cell vitality, increased apoptosis and also downregulated epithelial to mesenchymal transition (EMT) phenotype and the ability of invasion, but these processes were restored by the treatment of TNF-α. The oncogenic role of THRIL/TNF-α signal was also confirmed in the xenograft model of MG63 cells. Conclusion: Overexpressed THRIL and TNF-α promoted OS progression with efficient diagnostic and prognostic value. THRIL/TNF-α signal supported cell growth and EMT phenotype of OS cells in vitro and in vivo.

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“…At this point, again, the validity of the concept of the use of co-drugs in UFs should be emphasized. Hopefully, the future research will bring the opportunity to use patient-tailored multivalent therapies with the modulation of selected biochemical or genetic pathways [145]. In our opinion, much of the current research on UFs should focus on which growth factors, cytokines or miRNAs are most frequently associated with specific clinical conditions.…”

Section: Mirna and Uterine Fibroids-medical Treatmentmentioning

confidence: 99%

The Role of miRNA and Related Pathways in Pathophysiology of Uterine Fibroids—From Bench to Bedside

Ciebiera

Włodarczyk

Zgliczyński

et al. 2020

IJMS

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Uterine fibroids (UFs) are the most common benign tumors of the female genital tract. Their prevalence usually is estimated at 30–40%, but may reach up to 70–80% in predisposed groups of women. UFs may cause various clinical issues which might constitute the major reason of the overall deterioration of the quality of life. The mechanisms leading to UFs formation and growth still remain poorly understood. The transformation of smooth muscle cells of the uterus into abnormal, immortal cells, capable of clonal division, is thought to be a starting point of all pathways leading to UF formation. Micro-ribonucleic acids (miRNAs) are non-coding single-stranded RNAs about 22 nucleotides in length, that regulate gene expression. One of recent advances in this field is the comprehension of the role of miRNAs in tumorigenesis. Alterations in the levels of miRNAs are related to the formation and growth of several tumors which show a distinct miRNA signature. The aim of this review is to summarize the current data about the role of miRNAs in the pathophysiology of UFs. We also discuss future directions in the miRNA research area with an emphasis on novel diagnostic opportunities or patient-tailored therapies. In our opinion data concerning the regulation of miRNA and its gene targets in the UFs are still insufficient in comparison with gynecological malignancies. The potential translational use of miRNA and derived technologies in the clinical care is at the early phase and needs far more evidence. However, it is one of the main areas of interest for the future as the use of miRNAs in the diagnostics and treatment of UFs is a new and exciting opportunity.

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The Role of Tumor Necrosis Factor α in the Biology of Uterine Fibroids and the Related Symptoms

Cited by 58 publications

References 206 publications

Inflammatory Markers in Dysmenorrhea and Therapeutic Options

Inflammatory Markers in Dysmenorrhea and Therapeutic Options

<p>Upregulated lncRNA THRIL/TNF-α Signals Promote Cell Growth and Predict Poor Clinical Outcomes of Osteosarcoma</p>

The Role of miRNA and Related Pathways in Pathophysiology of Uterine Fibroids—From Bench to Bedside

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