SOX12 Promotes Thyroid Cancer Cell Proliferation and Invasion by Regulating the Expression of POU2F1 and POU3F1

Su, Zhenxi; Bao, Wenqing; Yang, Guanghua; Liu, Jianping; Zhao, Bin

doi:10.3349/ymj.2022.63.6.591

Cited by 9 publications

(5 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The regulation on TUNEL-positive cells seems important in the control of tumor progression of UC-CRC [ 36 ]. In line with previous studies, we demonstrated that Pou3f1 inhibition reduced pro-oncogenic cytokine production, suppressed cell proliferation and increased cell death in UC-CRC [ 22 , 37 ].…”

Section: Discussionsupporting

confidence: 92%

Pou3f1 mediates the effect of Nfatc3 on ulcerative colitis-associated colorectal cancer by regulating inflammation

et al. 2022

View full text Add to dashboard Cite

Background Ulcerative colitis-associated colorectal cancer (UC-CRC) is an important complication of ulcerative colitis. Pou3f1 (POU class 3 homeobox 1) is a critical regulator for developmental events and cellular biological processes. However, the role of Pou3f1 in the development of UC-CRC is unclear. Methods In vivo, a UC-CRC mouse model was induced by azoxymethane (AOM) and dextran sulfate sodium (DSS). Body weight, colon length, mucosal damage, tumor formation, and survival rate were assessed to determine the progression of UC-CRC. Western blot, quantitative real-time PCR, ELISA, immunohistochemistry, immunofluorescence and TUNEL were performed to examine the severity of inflammation and tumorigenesis. In vitro, LPS-treated mouse bone marrow-derived macrophages (BMDMs) and RAW264.7 cells were used to study the role of Pou3f1 in inflammation. ChIP and luciferase reporter assays were used to confirm the interaction between Nfatc3 and Pou3f1. Results Pou3f1 expression was increased in the colons of UC-CRC mice, and its inhibition attenuated mucosal injury, reduced colon tumorigenesis and increased survival ratio. Knockdown of Pou3f1 suppressed cell proliferation and increased cell death in colon tumors. Both the in vivo and in vitro results showed that Pou3f1 depletion reduced the production of proinflammation mediators. In addition, ChIP and luciferase reporter assays demonstrated that Nfatc3 directly bound with the Pou3f1 promoter to induce its expression. The effect of Nfatc3 on the inflammatory response in macrophages was suppressed by Pou3f1 knockdown. Conclusion Overall, it outlines that Pou3f1 mediates the role of Nfatc3 in regulating macrophage inflammation and carcinogenesis in UC-CRC development.

show abstract

Section: Discussionsupporting

confidence: 92%

Pou3f1 mediates the effect of Nfatc3 on ulcerative colitis-associated colorectal cancer by regulating inflammation

et al. 2022

View full text Add to dashboard Cite

show abstract

“…SOX12 knockdown inhibits the expression of POU2F1, POU3F1, and POU2F1. POU3F1 can reverse the effects of SOX12 knockdown on thyroid cancer cells, indicating their role in the progression of thyroid cancer [Su et al, 2022].…”

Section: Discussionmentioning

confidence: 99%

Higher-order correction of persistent batch effects in correlation networks

Micheletti,

Schlauch,

Quackenbush

et al. 2023

Preprint

View full text Add to dashboard Cite

Systems biology methods often rely on correlations in gene expression profiles to infer co-expression networks, commonly used as input for gene regulatory network inference or to identify functional modules of co-expressed or co-regulated genes. While systematic biases, including batch effects, are known to induce spurious associations and confound differential gene expression analyses (DE), the impact of batch effects on gene co-expression has not been fully explored. Methods have been developed to adjust expression values, ensuring conditional independence of mean and variance from batch or other covariates for each gene. These adjustments have been shown to improve the fidelity of DE analysis. However, these methods do not address the potential for spurious differential co-expression (DC) between groups. Consequently, uncorrected, artifactual DC can skew the correlation structure, leading network inference methods that use gene co-expression to identify false, nonbiological associations, even when the input data is corrected using standard batch correction.In this work, we demonstrate the persistence of confounders in covariance after standard batch correction using synthetic and real-world gene expression data examples. Subsequently, we introduce Co-expression Batch Reduction Adjustment (COBRA), a method for computing a batch-corrected gene co-expression matrix based on estimating a conditional covariance matrix. COBRA estimates a reduced set of parameters expressing the co-expression matrix as a function of the sample covariates, allowing control for continuous and categorical covariates. COBRA is computationally efficient, leveraging the inherently modular structure of genomic data to estimate accurate gene regulatory associations and facilitate functional analysis for high-dimensional genomic data.

show abstract

“…The circular RNA FNLA acts as a sponge for miR-149-5p, a microRNA that suppresses MMP9, thereby indirectly increasing MMP9 levels and promoting tumor invasion and metastasis [38]. Another pathway involves the SOX12 transcription factor, which activates the expression of POU2F1 and POU3F1, subsequently increasing the expression of MMP9 and promoting the invasion and metastasis of PTC cells [39]. Similarly, the long non-coding RNA DUXAP10 upregulates the Akt/mTOR signaling pathway, leading to increased MMP9 expression and promoting tumor progression and metastasis [40].…”

Section: Functional Analysis Of Mmp9 and Mir-145mentioning

confidence: 99%

Matrix Metalloproteinase 9/microRNA-145 Ratio: Bridging Genomic and Immunological Variabilities in Thyroid Cancer

Toraih,

Hussein,

Al Ageeli

et al. 2023

Biomedicines

View full text Add to dashboard Cite

Matrix metalloproteinase 9 (MMP9) and microRNA-145 (miR-145) have emerged as essential biomarkers in thyroid cancer progression and metastasis. However, their combined evaluation and clinical utility as a unified prognostic marker across diverse thyroid cancer subgroups remain unexplored. We investigated the diagnostic and prognostic value of the MMP9/miR-145 ratio in thyroid cancer, hypothesizing it may overcome inter-patient heterogeneity and serve as a versatile biomarker regardless of genetic mutations or autoimmune status. MMP9 and miR-145 expressions were analyzed in 175 paired papillary thyroid cancer (PTC) and normal tissues. Plasma levels were assessed perioperatively and longitudinally over 12–18 months in 86 matched PTC patients. The associations with clinicopathological parameters and patient outcomes were evaluated. MMP9 was upregulated, and miR-145 downregulated in cancer tissues, with a median MMP9/miR-145 ratio 17.6-fold higher versus controls. The tissue ratio accurately diagnosed thyroid malignancy regardless of BRAF mutation or Hashimoto’s thyroiditis status, overcoming genetic and autoimmune heterogeneity. A high preoperative circulating ratio predicted aggressive disease features, including lymph node metastasis, extrathyroidal extension, progression/relapse, and recurrence. Although the preoperative plasma ratio was elevated in patients with unfavorable outcomes, it had limited utility for post-surgical monitoring. In conclusion, the MMP9/miR-145 ratio is a promising biomarker in PTC that bridges genetic and immunological variabilities, enhancing preoperative diagnosis and prognostication across diverse patient subgroups. It accurately stratifies heterogenous cases by aggressiveness. The longitudinal trends indicate decreasing applicability for post-thyroidectomy surveillance. Further large-scale validation and protocol standardization can facilitate clinical translation of the MMP9/miR-145 ratio to guide personalized thyroid cancer management.

show abstract

SOX12 Promotes Thyroid Cancer Cell Proliferation and Invasion by Regulating the Expression of POU2F1 and POU3F1

Cited by 9 publications

References 33 publications

Pou3f1 mediates the effect of Nfatc3 on ulcerative colitis-associated colorectal cancer by regulating inflammation

Pou3f1 mediates the effect of Nfatc3 on ulcerative colitis-associated colorectal cancer by regulating inflammation

Higher-order correction of persistent batch effects in correlation networks

Matrix Metalloproteinase 9/microRNA-145 Ratio: Bridging Genomic and Immunological Variabilities in Thyroid Cancer

Contact Info

Product

Resources

About