Overexpression of LncRNA MNX1-AS1/PPFIA4 Activates AKT/HIF-1α Signal Pathway to Promote Stemness of Colorectal Adenocarcinoma Cells

Sun, Qi; Gui, Zhifu; Zhao, Zhenguo; Xu, Wenlong; Zhu, Jinming; Gao, Chun-Dong; Zhao, Wei; Hu, Hao

doi:10.1155/2022/8303409

Cited by 3 publications

(5 citation statements)

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“…This interaction protects HuR from polyubiquitination and proteasomal degradation, highlighting a crucial mechanism by which GMDS-AS1 contributes to the stabilization of proteins involved in cancer cell proliferation ( 61 ). The lncRNA MNX1-AS1/PPFIA4 activates the downstream AKT/HIF-1α signaling pathway to promote COAD proliferation ( 166 ). NEAT1 can regulate the miR-448/ZEB1 axis ( 167 ), and also directly acts as a molecular sponge for miR-216b, which in turn activates YY1 to promote CRC proliferation ( 168 ).…”

Section: Regulation Of Cell Proliferation By Lncrnasmentioning

confidence: 99%

“…Tang et al.’s study suggests that MIR497HG, as a ceRNA regulating the miR-3918/ACTG2 axis, plays a key role in CRC cell migration and invasion ( 218 ). MNX1-AS1 regulates miR-744-5p ( 165 ) or the PPFIA4/AKT/HIF-1α axis ( 166 ), playing a critical role in the invasion and migration of CRC cells.NEAT1 promotes the expression of ZEB1 by targeting miR-448 ( 167 ), or enhances the proliferation and invasion of CRC through the miR-216b/YY1 axis ( 168 ). Guan et al.…”

Section: Lncrnas Regulate Invasion and Metastasismentioning

confidence: 99%

“…reported that PPFIA4 mediates the expression of lncRNA MNX1-AS1 and affects the stemness of COAD cells. The MNX1-AS1/PPFIA4 activates the downstream AKT/HIF-1α signaling pathway to promote the progression of COAD ( 166 ). TDRG1 levels are significantly upregulated in 3D non-adherent spheroids derived from parental CRC cells.…”

Section: Lncrnas Regulate Cancer Cell Stemnessmentioning

confidence: 99%

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The functions and mechanisms of long non-coding RNA in colorectal cancer

Lin,

Zhao,

et al. 2024

Front. Oncol.

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CRC poses a significant challenge in the global health domain, with a high number of deaths attributed to this disease annually. If CRC is detected only in its advanced stages, the difficulty of treatment increases significantly. Therefore, biomarkers for the early detection of CRC play a crucial role in improving patient outcomes and increasing survival rates. The development of a reliable biomarker for early detection of CRC is particularly important for timely diagnosis and treatment. However, current methods for CRC detection, such as endoscopic examination, blood, and stool tests, have certain limitations and often only detect cases in the late stages. To overcome these constraints, researchers have turned their attention to molecular biomarkers, which are considered a promising approach to improving CRC detection. Non-invasive methods using biomarkers such as mRNA, circulating cell-free DNA, microRNA, LncRNA, and proteins can provide more reliable diagnostic information. These biomarkers can be found in blood, tissue, stool, and volatile organic compounds. Identifying molecular biomarkers with high sensitivity and specificity for the early and safe, economic, and easily measurable detection of CRC remains a significant challenge for researchers.

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Section: Regulation Of Cell Proliferation By Lncrnasmentioning

confidence: 99%

Section: Lncrnas Regulate Invasion and Metastasismentioning

confidence: 99%

Section: Lncrnas Regulate Cancer Cell Stemnessmentioning

confidence: 99%

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The functions and mechanisms of long non-coding RNA in colorectal cancer

Lin,

Zhao,

et al. 2024

Front. Oncol.

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“…Colonies formed in each group were observed, and the number of colonies with more than 10 cells was counted by photographing them under a microscope (Olympus). Colony formation rate was calculated as previous reports (Liu et al, 2021;Sun et al, 2022).…”

Section: Colony Formation Assaymentioning

confidence: 99%

“…The proteins were visualized by a DAB immunohistochemistry color development kit (Sangon Biotech, China) and photographed using a gel imaging analysis system (Thermo Fisher Scientifi). Relative protein levels were calculated by ImageJ as previous report (Sun et al, 2022).…”

Section: Western Blot Assaymentioning

confidence: 99%

Second generation androgen receptor antagonist, TQB3720 abrogates prostate cancer growth via AR/GPX4 axis activated ferroptosis

Zhang

Xie²,

Zhang³

et al. 2023

Front. Pharmacol.

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Purpose: Prostate cancer (PCa) poses a great threat to humans. The study aimed to evaluate the potential of TQB3720 in promoting ferroptosis to suppress prostate cancer, providing a theoretical basis for PCa therapy.Methods: PCa cells and nude mice models were divided into TQB3720, enzalutamide (ENZ), and control groups. Sulforhodamine B assay, colony formation assessment, organoids culture system, and the CCK8 assay were used for detecting proliferation. Western blot assay was processed to detect the expression of androgen receptor (AR), ferroptosis, and apoptosis-related genes. Flow cytometry was applied to measure the intracellular ROS levels. ELISA was performed to determine the cellular oxidized glutathione (GSSG) and malondialdehyde (MDA) levels. RT-qPCR was conducted to detect the mRNA expression of genes in AR signaling. BODIPYTM™ 581/591 was processed for detection of intracellular lipid peroxidation levels. The interaction of AR with other translational factor complex proteins was explored using Co-immunoprecipitation (Co-IP), and the chromatin immunoprecipitation (ChIP) assay was performed to detect the binding of AR-involved translational complex to downstream genes promoter. Luciferase reporter assay was conducted to examine the translation activity of GPX4 promoter, and immunohistochemistry (IHC) was conducted to analyze the levels of c-MYC, Ki-67 and AR in TQB3720-treated cancer tissues.Results: Here, we found TQB3720 inhibits the growth of prostate cancer in vitro and in vivo. TQB3720 treatment induced intracellular levels of GSSG and MDA significantly, by which hints AR antagonist caused ferroptosis-related cell death. Moreover, molecular evidence shown TQB3720 regulates downstream of AR signaling by binding AR resulting in inhibition of AR entry into the nucleus. Additional, we also proved that TQB3720 abrogates the interaction between AR and SP1 and leads to decrease GPX4 transcription.Conclusion: TQB3720 promotes ferroptosis in prostate cancer cells by reducing the AR/SP1 transcriptional complex binding to GPX4 promoter. As a result, it is suggested to be a potential drug for clinic prostate cancer treatment.

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