TRIM38 suppresses migration, invasion, metastasis, and proliferation in non-small cell lung cancer (NSCLC) via regulating the AMPK/NF-κB/NLRP3 pathway

Zhang, Kaihua; Lin, Guihu; Nie, Zhenkai; Jin, S.; Bing, Xiaohan; Li, Zhantao; Li, Mingru

doi:10.1007/s11010-023-04823-y

Cited by 3 publications

(1 citation statement)

References 40 publications

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“…PGC1-α is a mitochondriarelated gene transcriptional coactivator, which acts as a nuclear transcription coactivator to increase transcriptional efficiency by binding to other coactivators to different target genes, thereby regulating important physiological processes such as fatty acid oxidation, oxidative phosphorylation, and mitochondrial biogenesis [20] . PGC1-α activates the TFAM of mitochondrial DNA, and Together with Mitochondrial Transcription Factor B (TFBM) and mitochondrial RNA polymerase, it forms a transcriptional initiation complex that regulates mitochondrial biogenesis and function [21] . It has been demonstrated that over activation of the AMPK/PGC-1α signaling pathway is crucial in controlling the proliferation, survival, and aggressiveness of endometrial cancer cells, breast cancer cells, and gastric cancer cells [22] .…”

Section: Groupmentioning

confidence: 99%

Effect of Erlotinib Combined with Radiotherapy on Proliferation and Apoptosis of Human Non-Small Cell Lung Cancer Cells and its Possible Mechanism Exploration

Li,

Ma,

Diao

et al. 2024

IJPS

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To explore the effects and possible mechanisms of erlotinib combined with radiotherapy on the proliferation and apoptosis of human non-small cell lung cancer cells. Blank control group, non-small cell lung cancer group and erlotinib group were set cells in the blank control group were human bronchial epithelioid cells without any treatment and cultured routinely. The proliferation ability of the cells in the three groups was detected by cell counting kit-8, Western blot was used to assess protein expression, quantitative polymerase chain reaction was used to measure messenger ribonucleic acid expression, and Transwell was used to determine metastatic potential. The quantity of migrating cells and the rate of cell growth of non-small cell lung cancer group were higher than that of blank control group; the cell metastasis activity number of erlotinib group were reduced than that of non-small cell lung cancer group. The cell invasion number of non-small cell lung cancer group was higher than blank control group; erlotinib group was reduced than that of non-small cell lung cancer group. The overall apoptosis rate was higher than the non-small cell lung cancer group. The apoptotic proteins Fas, B-cell lymphoma 2-associated X protein and Fas ligand were higher in the erlotinib group than in the non-small cell lung cancer group, and the B-cell lymphoma 2 was reduced than the nonsmall cell lung cancer group. The 5' adenosine monophosphate-activated protein kinase and peroxisome proliferator-activated receptor coactivator-1 alpha in the non-small cell lung cancer group were reduced than the blank control group and erlotinib group were higher than the non-small cell lung cancer group. The protein mitogen-activated protein kinase and peroxisome proliferator-activated receptor coactivator-1 alpha in the non-small cell lung cancer group were reduced than the blank control group and erlotinib group were higher than those in the non-small cell lung cancer group. The mechanism of erlotinib's capacity to lower the viability of non-small cell lung cancer cells, block their proliferation, migration, and invasion ability, and induce apoptosis may be connected to the control of the 5' adenosine monophosphate-activated protein kinase/ peroxisome proliferator-activated receptor coactivator-1 alpha signaling pathway.

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Section: Groupmentioning

confidence: 99%

Effect of Erlotinib Combined with Radiotherapy on Proliferation and Apoptosis of Human Non-Small Cell Lung Cancer Cells and its Possible Mechanism Exploration

Li,

Ma,

Diao

et al. 2024

IJPS

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Multifaceted role of TRIM28 in health and disease

Maghsoudloo,

Mokhtari,

Jamali

et al. 2024

MedComm

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The TRIM (tripartite motif) family, with TRIM28 as a key member, plays a vital role in regulating health and disease. TRIM28 contains various functional domains essential for transcriptional regulation, primarily through its interaction with KRAB‐ZNF proteins, which influence chromatin remodeling and gene expression. Despite extensive research, the precise mechanisms by which TRIM28 impacts health and disease remain elusive. This review delves into TRIM28’s multifaceted roles in maintaining health, contributing to a variety of diseases, and influencing cancer progression. In cancers, TRIM28 exhibits a dual nature, functioning as both a tumor promoter and suppressor depending on the cellular context and cancer type. The review also explores its critical involvement in processes such as DNA repair, cell cycle regulation, epithelial‐to‐mesenchymal transition, and the maintenance of stem cell properties. By uncovering TRIM28’s complex roles across different cancers and other diseases, this review underscores its potential as a therapeutic target. The significance of TRIM28 as a versatile regulator opens the door to innovative therapeutic strategies, particularly in cancer treatment and the management of other diseases. Ongoing research into TRIM28 may yield key insights into disease progression and novel treatment options.

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Therapeutic Significance of NLRP3 Inflammasome in Cancer: Friend or Foe?

Jalali,

Mitchell,

Pompoco

et al. 2024

IJMS

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Besides various infectious and inflammatory complications, recent studies also indicated the significance of NLRP3 inflammasome in cancer progression and therapy. NLRP3-mediated immune response and pyroptosis could be helpful or harmful in the progression of cancer, and also depend on the nature of the tumor microenvironment. The activation of NLRP3 inflammasome could increase immune surveillance and the efficacy of immunotherapy. It can also lead to the removal of tumor cells by the recruitment of phagocytic macrophages, T-lymphocytes, and other immune cells to the tumor site. On the other hand, NLRP3 activation can also be harmful, as chronic inflammation driven by NLRP3 supports tumor progression by creating an environment that facilitates cancer cell proliferation, migration, invasion, and metastasis. The release of pro-inflammatory cytokines such as IL-1β and IL-18 can promote tumor growth and angiogenesis, while sustained inflammation may lead to immune suppression, hindering effective anti-tumor responses. In this review article, we discuss the role of NLRP3 inflammasome-mediated inflammatory response in the pathophysiology of various cancer types; understanding this role is essential for the development of innovative therapeutic strategies for cancer growth and spread.

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TRIM38 suppresses migration, invasion, metastasis, and proliferation in non-small cell lung cancer (NSCLC) via regulating the AMPK/NF-κB/NLRP3 pathway

Cited by 3 publications

References 40 publications

Effect of Erlotinib Combined with Radiotherapy on Proliferation and Apoptosis of Human Non-Small Cell Lung Cancer Cells and its Possible Mechanism Exploration

Effect of Erlotinib Combined with Radiotherapy on Proliferation and Apoptosis of Human Non-Small Cell Lung Cancer Cells and its Possible Mechanism Exploration

Multifaceted role of TRIM28 in health and disease

Therapeutic Significance of NLRP3 Inflammasome in Cancer: Friend or Foe?

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