The suppression of OTUD7B by miR‐491‐5p enhances the ubiquitination of VEGFA to suppress vascular mimicry in non‐small cell lung cancer DOI
Xiaofei Chen,

Lijun He,

Hai Zhong

и другие.

The Journal of Gene Medicine, Год журнала: 2024, Номер 26(10)

Опубликована: Окт. 1, 2024

Abstract Background Non‐small cell lung cancer (NSCLC) is the main type of with high morbidity and mortality. Vascular mimicry (VM), a distinct microcirculation model in tumors that differs from classical angiogenesis, strongly associated poor clinical outcomes patients. miR‐491‐5p has been reported to prevent NSCLC progression, including proliferation, metastasis, angiogenesis. However, effect mechanism on VM have not studied NSCLC. Methods The expression was detected by quantitative reverse transcription PCR (qPCR) fluorescence situ hybridization (FISH). Cell counting kit‐8 (CCK‐8) 5‐ethynyl‐2′‐deoxyuridine (EdU) staining assays were used examine growth. Tube formation assay assess cells. Immunohistochemistry (IHC) western blot performed detect protein expression. Immunoprecipitation confirm interaction between OTU deubiquitinase 7B (OTUD7B) vascular endothelial growth factor A (VEGFA), level ubiquitinated VEGFA. nude mouse tumorigenesis evaluate carcinogenic capacity cells vivo. Luciferase reporter identify potential target miR‐491‐5p. Results MiR‐491‐5p found downregulated tissues, deficiency mimics suppressed viability, migration, VM. Conversely, an inhibitor had opposite effect. OTUD7B, deubiquitinase, identified as downstream luciferase indicated directly binds 3′UTR OTUD7B. Moreover, caused significant reduction OTUD7B cells, stabilized protein. In addition, overexpression promoted VM, similar effects Further exploration revealed interacts VEGFA miR‐491‐5p‐OTUD7B axis modulates ubiquitination rescue experiment compromised inhibitory cellular function Conclusions Overall, our study first proved impedes suppressing OUTD7B promoting miR‐491‐5p/OTUD7B may be novel for antiangiogenic therapy

Язык: Английский

Targeting ferroptosis: a promising approach for treating lung carcinoma DOI Creative Commons
Ziyang Wu, Tao Zhang, Wei Zhong

и другие.

Cell Death Discovery, Год журнала: 2025, Номер 11(1)

Опубликована: Янв. 29, 2025

Abstract Lung carcinoma incidence and fatality rates remain among the highest on a global scale. The efficacy of targeted therapies immunotherapies is commonly compromised by emergence drug resistance other factors, resulting in lack durable therapeutic benefits. Ferroptosis, distinct pattern cell death marked buildup iron-dependent lipid peroxides, has been shown to be novel potentially more effective treatment for lung carcinoma. However, mechanism regulatory network ferroptosis are exceptionally complex, many unanswered questions remain. In addition, research diagnosis cancer growing exponentially. Therefore, it necessary provide thorough summary latest advancements field ferroptosis. Here, we comprehensively analyze mechanisms underlying preconditions ferroptosis, defense system, associated molecular networks. potential strategies also highlighted. Targeting improves tumor enhances effectiveness drugs immunotherapies. These findings may shed fresh light management carcinoma, as well development related

Язык: Английский

Процитировано

0
The Potential Role of Non-coding RNAs in Regulating Ferroptosis in Cancer: Mechanisms and Application Prospects DOI

Ming-Yuan Cao,

Zhendong Zhang,

Xin-Rui Hou

и другие.

Anti-Cancer Agents in Medicinal Chemistry, Год журнала: 2024, Номер 24(16), С. 1182 - 1196

Опубликована: Июль 18, 2024

: Cancer is the second leading cause of death globally. Despite some successes, conventional cancer treatments are insufficient to address growing problem drug resistance in tumors and achieve efficient treatment outcomes. Therefore, there an urgent need explore new therapeutic options. Ferroptosis, a type iron- reactive oxygen species-dependent regulated cell death, has been closely associated with development progression. Non-coding RNAs (ncRNAs) class that do not code for proteins, studies have demonstrated their involvement regulation ferroptosis cancer. This review aims molecular regulatory mechanisms ncRNAs involved emphasize feasibility as novel strategies We conducted systematic extensive literature using PubMed, Google Scholar, Web Science, various other sources identify relevant on ferroptosis, ncRNAs, A deeper understanding could facilitate strategies.

Язык: Английский

Процитировано

0
The suppression of OTUD7B by miR‐491‐5p enhances the ubiquitination of VEGFA to suppress vascular mimicry in non‐small cell lung cancer DOI
Xiaofei Chen,

Lijun He,

Hai Zhong

и другие.

The Journal of Gene Medicine, Год журнала: 2024, Номер 26(10)

Опубликована: Окт. 1, 2024

Abstract Background Non‐small cell lung cancer (NSCLC) is the main type of with high morbidity and mortality. Vascular mimicry (VM), a distinct microcirculation model in tumors that differs from classical angiogenesis, strongly associated poor clinical outcomes patients. miR‐491‐5p has been reported to prevent NSCLC progression, including proliferation, metastasis, angiogenesis. However, effect mechanism on VM have not studied NSCLC. Methods The expression was detected by quantitative reverse transcription PCR (qPCR) fluorescence situ hybridization (FISH). Cell counting kit‐8 (CCK‐8) 5‐ethynyl‐2′‐deoxyuridine (EdU) staining assays were used examine growth. Tube formation assay assess cells. Immunohistochemistry (IHC) western blot performed detect protein expression. Immunoprecipitation confirm interaction between OTU deubiquitinase 7B (OTUD7B) vascular endothelial growth factor A (VEGFA), level ubiquitinated VEGFA. nude mouse tumorigenesis evaluate carcinogenic capacity cells vivo. Luciferase reporter identify potential target miR‐491‐5p. Results MiR‐491‐5p found downregulated tissues, deficiency mimics suppressed viability, migration, VM. Conversely, an inhibitor had opposite effect. OTUD7B, deubiquitinase, identified as downstream luciferase indicated directly binds 3′UTR OTUD7B. Moreover, caused significant reduction OTUD7B cells, stabilized protein. In addition, overexpression promoted VM, similar effects Further exploration revealed interacts VEGFA miR‐491‐5p‐OTUD7B axis modulates ubiquitination rescue experiment compromised inhibitory cellular function Conclusions Overall, our study first proved impedes suppressing OUTD7B promoting miR‐491‐5p/OTUD7B may be novel for antiangiogenic therapy

Язык: Английский

Процитировано

0