In search of new stratification strategies: Tissue proteomic profiling of papillary thyroid microcarcinoma in patients with localized disease and lateral neck metastases DOI Creative Commons

Filip Matovinović,

Rudjer Novak,

Stela Hrkač

и другие.

Research Square (Research Square), Год журнала: 2023, Номер unknown

Опубликована: Июль 19, 2023

Abstract Introduction: Papillary thyroid carcinomas (PTC) are the most common malignancies that often diagnosed as microcarcinomas when tumour is less than one centimetre in diameter. Currently, there no valid stratification strategies would reliably assess risk of lateral neck metastases and optimize surgical treatment. Materials methods: Aiming to find potential tissue biomarkers metastatic potential, we conducted a cross-sectional proteomic study on formalin-fixed paraffin-embedded tissues (N = 10) non-metastatic papillary microcarcinoma patients. Samples were analysed individually using liquid-chromatography / mass spectrometry, differentially expressed proteins (DEP) functionally annotated. Results: We identified five overexpressed DEPs group (EPB41L2, CSE1L, GLIPR2, FGA FGG) with known association biology. Using bioinformatics tools, found markedly different profiles significantly enriched biological processes between two groups. Conclusion: The might have role for PTC metastases. However, further prospective research needed order confirm our findings.

Язык: Английский

Sirtuin 5‐Mediated Desuccinylation of ALDH2 Alleviates Mitochondrial Oxidative Stress Following Acetaminophen‐Induced Acute Liver Injury DOI Creative Commons
Q C Yu, Jiakai Zhang, Jiye Li

и другие.

Advanced Science, Год журнала: 2024, Номер 11(39)

Опубликована: Авг. 19, 2024

Abstract Acetaminophen (APAP) overdose is a major cause of drug‐induced liver injury. Sirtuins 5 (SIRT5) has been implicated in the development various diseases. However, its involvement APAP‐induced acute injury (AILI) remains unclear. The present study aimed to explore role SIRT5 AILI. expression dramatically downregulated by APAP administration mouse livers and AML12 hepatocytes. deficiency not only exacerbates inflammatory response, but also worsens mitochondrial oxidative stress. Conversely, opposite pathological biochemical changes are observed mice with overexpression. Mechanistically, quantitative succinylome analysis site mutation experiments revealed that desuccinylated aldehyde dehydrogenase 2 (ALDH2) at lysine 385 maintained enzymatic activity ALDH2, resulting suppression inflammation Furthermore, succinylation ALDH2 abolished protective effect against AILI, AILI dependent on desuccinylation K385. Finally, virtual screening natural compounds Puerarin promoted desuccinylase further attenuated Collectively, showed SIRT5‐ALDH2 axis plays critical progression might be strategy for therapeutic intervention.

Язык: Английский

Процитировано

9

SIRT7 promotes the proliferation and migration of anaplastic thyroid cancer cells by regulating the desuccinylation of KIF23 DOI Creative Commons
Yongkang Wu, Weijie Chen, Huilai Miao

и другие.

BMC Cancer, Год журнала: 2024, Номер 24(1)

Опубликована: Фев. 15, 2024

Abstract Objective This study was designed to investigate the regulatory effects of kinesin family member (KIF) 23 on anaplastic thyroid cancer (ATC) cell viability and migration underlying mechanism. Methods Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) used analyze levels KIF23 in ATC cells. Besides, sirtuin (SIRT) 7 cells were detected using counting kit-8, transwell wound healing assays. The interaction between SIRT7 evaluated by co-immunoprecipitation (Co-IP) assay. succinylation (succ) analyzed western blot. Results expression upregulated Silencing suppressed 8505C BCPAP KIF23-succ level decreased interacted with inhibit at K537 site human embryonic kidney (HEK)-293T Overexpression enhanced protein stability HEK-293T overexpression promoted cells, which partly blocked silenced SIRT7. Conclusions proliferation regulating desuccinylation KIF23.

Язык: Английский

Процитировано

8

Targeting succinylation-mediated metabolic reprogramming as a potential approach for cancer therapy DOI Open Access
Zhenya Liu, Runxian Wang, Yunshan Wang

и другие.

Biomedicine & Pharmacotherapy, Год журнала: 2023, Номер 168, С. 115713 - 115713

Опубликована: Окт. 16, 2023

Metabolic reprogramming is a common hallmark of cancers and involves alterations in many metabolic pathways during tumor initiation progression. However, the cancer-specific modulation requires further elucidation. Succinylation, newly identified protein posttranslational modification (PTM), participates cellular processes by transferring succinyl group to residue target protein, which related various pathological disorders including cancers. In recent years, there has been gradual increase number studies on regulation tumors succinylation. Notably, accumulating evidence suggests that succinylation can mediate cancer cell metabolism altering structure or activity metabolism-related proteins plays vital roles reprogramming. Furthermore, some antitumor drugs have linked succinylation-mediated tumor-associated metabolism. To better elucidate lysine mediated reprogramming, this review mainly summarizes effects tumors, focusing tumorigenesis development, will provide new directions for diagnosis as well possible therapeutic targets.

Язык: Английский

Процитировано

12

Galactia lindenii lectin type-II: Its potential use in thyroid cancer diagnosis DOI Creative Commons

Tania M. Cortázar,

Nelson Osorio,

Jinneth Acosta

и другие.

Acta Histochemica, Год журнала: 2025, Номер 127(2), С. 152250 - 152250

Опубликована: Апрель 7, 2025

Язык: Английский

Процитировано

0

In search of new stratification strategies: tissue proteomic profiling of papillary thyroid microcarcinoma in patients with localized disease and lateral neck metastases DOI

Filip Matovinović,

Rudjer Novak,

Stela Hrkač

и другие.

Journal of Cancer Research and Clinical Oncology, Год журнала: 2023, Номер 149(19), С. 17405 - 17417

Опубликована: Окт. 20, 2023

Язык: Английский

Процитировано

6

Epigenetic Targets and Their Inhibitors in Thyroid Cancer Treatment DOI Creative Commons
Ke Zhang, Junyao Wang,

Ziyan He

и другие.

Pharmaceuticals, Год журнала: 2023, Номер 16(4), С. 559 - 559

Опубликована: Апрель 7, 2023

Although biologically targeted therapies based on key oncogenic mutations have made significant progress in the treatment of locally advanced or metastatic thyroid cancer, challenges drug resistance are urging us to explore other potentially effective targets. Herein, epigenetic modifications including DNA methylation, histone modifications, non-coding RNAs, chromatin remodeling and RNA alterations, reviewed therapeutic agents for such as DNMT (DNA methyltransferase) inhibitors, HDAC (histone deacetylase) BRD4 (bromodomain-containing protein 4) KDM1A (lysine demethylase 1A) inhibitors EZH2 (enhancer zeste homolog 2) updated. We conclude that epigenetics is promising a target cancer further clinical trials warranted.

Язык: Английский

Процитировано

5

Unraveling the Post-Translational Modifications and therapeutical approach in NSCLC pathogenesis DOI Creative Commons
Pooja Gulhane, Shailza Singh

Translational Oncology, Год журнала: 2023, Номер 33, С. 101673 - 101673

Опубликована: Апрель 14, 2023

Non-Small Cell Lung Cancer (NSCLC) is the most prevalent kind of lung cancer with around 85% total cases. Despite vast therapies being available, survival rate low (5 year 15%) making it essential to comprehend mechanism for NSCLC cell and progression. The plethora evidences suggests that Post Translational Modification (PTM) such as phosphorylation, methylation, acetylation, glycosylation, ubiquitination SUMOylation are involved in various types progression metastasis including NSCLC. Indeed, an in-depth understanding PTM associated biology will provide novel therapeutic targets insight into current sophisticated paradigm. Herein, we reviewed key PTMs, epigenetic modulation, PTMs crosstalk along proteogenomics analyze also, highlighted how epi‑miRNA, miRNA inhibitors modulators serve promising therapeutics.

Язык: Английский

Процитировано

4

Epigenetic Regulation of Fungal Secondary Metabolites for the Enhancement of Therapeutically Active Compounds DOI
Shaurya Prakash,

Hemlata Kumari,

Minakshi

и другие.

Опубликована: Янв. 1, 2024

The microbial flora has always been a center of interest for the identification novel bioactive secondary metabolites (SMs) used against diversity infections and ailments. These compounds are produced by hosts in response to different stress conditions. Novobiocin naturally synthesized Streptomyces spheroids, Echinocandin B from Emericella rugulosa, Penicillin Penicillium chrysogenum, Gentamycin Micromonospora purpurea such examples. In nature, genes, either cryptic or compounds, synthesize trace amounts under specific environmental conditions, physiological conditions which make their bioavailability scarcer. Different strategies as induced stimuli, cloning genes control strong promoters, downregulating expression negative regulators, epigenetic manipulations, etc. have tried increase SM bioavailability. posttranslational modifications histones proteins render regulate also implied. Here, this chapter, we emphasized regulation enhancement production therapeutically significant fungi. DNA wrapped around undergo that facilitate chromatin packaging loose (euchromatin) tight (heterochromatin). Such alterations epigenetically modulate responsible regulating metabolic events. Relevance approaches use Histone deacetylase inhibitors (HDACs) methyl transferase (DNMTs) concern fungal compounds. could be intrinsically programmed affected externally. studies provided supportive arguments about modifiers increasing act locally globally inducing repressing synthesis genes. earlier studied modulation metabolite For instance, 5-azacytidine, hydralazine hydrochloride, trichostatin A, trapoxin B, chapter elaborates on more developed understanding histone activation/induction yield pharmacologically fungal-derived

Язык: Английский

Процитировано

1

LncRNA ZFAS1 promotes invasion of medullary thyroid carcinoma by enhancing EPAS1 expression via miR‐214‐3p/UCHL1 axis DOI Creative Commons
Wenjing Chen, Shaoqing Wang, Dongmei Wei

и другие.

Journal of Cell Communication and Signaling, Год журнала: 2024, Номер 18(2)

Опубликована: Апрель 12, 2024

Abstract lncRNA ZFAS1 was identified to facilitate thyroid cancer, but its role in medullary carcinoma (MTC) remains unknown. This study aimed unravel the potential function of this MTC by investigating involvement a ceRNA network that regulates invasion. Proliferation, invasion, and migration cells were evaluated using EdU staining Transwell assays. Immunoprecipitation (IP) assays, dual‐fluorescence reporter, RNA IP assays employed examine binding interaction among genes. Nude mice used explore vivo. EPAS1 upregulated MTC. Silencing inhibited cell proliferation invasion under hypoxic conditions, which reduced protein levels. UCHL1 knockdown increased ubiquitination. positively regulated expression miR‐214‐3p. Finally, silencing significantly repressed tumor formation metastasis LncRNA promotes upregulating via miR‐214‐3p/UCHL1 axis.

Язык: Английский

Процитировано

1

Ubiquitin-modifying enzymes in thyroid cancer:Mechanisms and functions DOI Creative Commons
Xingmin Xiong,

BenBen Huang,

Zhe Gan

и другие.

Heliyon, Год журнала: 2024, Номер 10(13), С. e34032 - e34032

Опубликована: Июль 1, 2024

Thyroid cancer is the most common malignant tumor of endocrine system, and evidence suggests that post-translational modifications (PTMs) epigenetic alterations play an important role in its development. Recently, there has been increasing linking dysregulation ubiquitinating enzymes deubiquitinases with thyroid cancer. This review aims to summarize our current understanding ubiquitination-modifying cancer, including their regulation oncogenic pathways proteins. The development progression requires further study, which will provide new insights into prevention, treatment novel agents.

Язык: Английский

Процитировано

1