We are analyzing https://link.springer.com/article/10.1007/s11010-022-04541-x.

Title:
ALKBH5 inhibits thyroid cancer progression by promoting ferroptosis through TIAM1–Nrf2/HO-1 axis | Molecular and Cellular Biochemistry
Description:
As a critical catalytic subunit of N6-methyladenosine (m6A) modification in messenger RNA, ALKBH5 has been reported to affect the progression of numerous tumors. However, the functions and mechanisms of ALKBH5 in thyroid cancer remain largely unknown. Relative mRNA and protein levels in thyroid cancer tissues and cells were detected by qRT-PCR and western blot, respectively. The proliferation and viability were evaluated using colony formation and CCK-8 assays. Intracellular iron level was measured by an iron colorimetric assay kit. ROS level was determined using CellRox Green reagent. TIAM1 mRNA m6A level was detected by MeRIP. Xenograft tumor growth was performed to examine the role of ALKBH5 in thyroid tumor growth in vivo. ALKBH5 was decreased in thyroid cancer tissues and cells. ALKBH5 overexpression inhibited thyroid cancer cell proliferation and increased the levels of Fe2+ and ROS and reduced the proteins expression of GPX4 and SLC7A11. Furthermore, overexpression of ALKBH5 inhibited TIAM1 expression by m6A modification, and overexpression of TIAM1 reversed the regulatory of oe-ALKBH5 on cell proliferation and ferroptosis in thyroid cancer. In addition, TIAM1 was elevated in thyroid cancer, and TIAM1 knockdown repressed thyroid cancer cell proliferation and promoted ferroptosis through regulating Nrf2/HO-1 axis. In addition, in vivo evidences also showed that ALKBH5 suppressed thyroid cancer progression by decreasing the m6A level of TIAM1. Our findings suggested that ALKBH5 inhibited thyroid cancer progression by inducing ferroptosis through m6A-TIAM1–Nrf2/HO-1 axis, suggesting ALKBH5 might be a potential target molecule for the treatment and diagnosis of thyroid cancer.
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Keywords {🔍}

pubmed, article, cancer, google, scholar, thyroid, cas, alkbh, central, ferroptosis, tiam, yang, cell, wang, expression, chen, progression, zhang, liu, inhibits, wei, cells, papillary, carcinoma, qrtpcr, tumor, nrf, axis, proliferation, access, mol, httpsdoiorgs, zhao, promotes, china, affiliated, university, privacy, cookies, content, data, information, research, guo, huang, jiang, rna, level, inhibited, metastasis,

Topics {✒️}

perk-nrf2-ho-1 signaling pathway microrna-26a-5p inhibits proliferation month download article/chapter tiam1–nrf2/ho-1 axis published m6a-tiam1–nrf2/ho-1 axis small-cell lung cancer tiam1–nrf2/ho-1 axis mirna-338-3p/rab23 axis nrf2/ho-1/nqo1 inhibition microrna-1271-5p/tiam1 suppresses regulating nrf2/ho-1 axis wnt/beta-catenin signaling a-guided epigenetic inhibition hypoxia-responsive tumor suppressor m6a-ck2alpha-mediated glycolysis hengyang medical college cellular biochemistry aims full article pdf papillary thyroid cancer nrf2/ho-1 axis mir-545-3p/slc7a11 signaling anaplastic thyroid cancer data availability thyroid cancer tissues thyroid cancer subtypes papillary thyroid carcinoma thyroid cancer cells alkbh5 inhibited autophagy s1 qrt-pcr analysis privacy choices/manage cookies related subjects clinical research center nrf2 inhibits ferroptosis tiam1 promotes chemoresistance thyroid tumor growth nrf2 inhibition reverses mediating wnt signaling alkbh5 suppresses malignancy attenuates tumor growth artesunate-induced ferroptosis neck cancer cells methyladenosine alkbh5 promotes differential microrna-signatures accepted manuscript version epithelial ovarian cancer colorectal cancer cells solid cancers rna methylation regulators med princ pract article molecular

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         headline:ALKBH5 inhibits thyroid cancer progression by promoting ferroptosis through TIAM1–Nrf2/HO-1 axis
         description:As a critical catalytic subunit of N6-methyladenosine (m6A) modification in messenger RNA, ALKBH5 has been reported to affect the progression of numerous tumors. However, the functions and mechanisms of ALKBH5 in thyroid cancer remain largely unknown. Relative mRNA and protein levels in thyroid cancer tissues and cells were detected by qRT-PCR and western blot, respectively. The proliferation and viability were evaluated using colony formation and CCK-8 assays. Intracellular iron level was measured by an iron colorimetric assay kit. ROS level was determined using CellRox Green reagent. TIAM1 mRNA m6A level was detected by MeRIP. Xenograft tumor growth was performed to examine the role of ALKBH5 in thyroid tumor growth in vivo. ALKBH5 was decreased in thyroid cancer tissues and cells. ALKBH5 overexpression inhibited thyroid cancer cell proliferation and increased the levels of Fe2+ and ROS and reduced the proteins expression of GPX4 and SLC7A11. Furthermore, overexpression of ALKBH5 inhibited TIAM1 expression by m6A modification, and overexpression of TIAM1 reversed the regulatory of oe-ALKBH5 on cell proliferation and ferroptosis in thyroid cancer. In addition, TIAM1 was elevated in thyroid cancer, and TIAM1 knockdown repressed thyroid cancer cell proliferation and promoted ferroptosis through regulating Nrf2/HO-1 axis. In addition, in vivo evidences also showed that ALKBH5 suppressed thyroid cancer progression by decreasing the m6A level of TIAM1. Our findings suggested that ALKBH5 inhibited thyroid cancer progression by inducing ferroptosis through m6A-TIAM1–Nrf2/HO-1 axis, suggesting ALKBH5 might be a potential target molecule for the treatment and diagnosis of thyroid cancer.
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            Nrf2/HO-1 pathway
            Biochemistry
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            Cardiology
            Cancer Research
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      headline:ALKBH5 inhibits thyroid cancer progression by promoting ferroptosis through TIAM1–Nrf2/HO-1 axis
      description:As a critical catalytic subunit of N6-methyladenosine (m6A) modification in messenger RNA, ALKBH5 has been reported to affect the progression of numerous tumors. However, the functions and mechanisms of ALKBH5 in thyroid cancer remain largely unknown. Relative mRNA and protein levels in thyroid cancer tissues and cells were detected by qRT-PCR and western blot, respectively. The proliferation and viability were evaluated using colony formation and CCK-8 assays. Intracellular iron level was measured by an iron colorimetric assay kit. ROS level was determined using CellRox Green reagent. TIAM1 mRNA m6A level was detected by MeRIP. Xenograft tumor growth was performed to examine the role of ALKBH5 in thyroid tumor growth in vivo. ALKBH5 was decreased in thyroid cancer tissues and cells. ALKBH5 overexpression inhibited thyroid cancer cell proliferation and increased the levels of Fe2+ and ROS and reduced the proteins expression of GPX4 and SLC7A11. Furthermore, overexpression of ALKBH5 inhibited TIAM1 expression by m6A modification, and overexpression of TIAM1 reversed the regulatory of oe-ALKBH5 on cell proliferation and ferroptosis in thyroid cancer. In addition, TIAM1 was elevated in thyroid cancer, and TIAM1 knockdown repressed thyroid cancer cell proliferation and promoted ferroptosis through regulating Nrf2/HO-1 axis. In addition, in vivo evidences also showed that ALKBH5 suppressed thyroid cancer progression by decreasing the m6A level of TIAM1. Our findings suggested that ALKBH5 inhibited thyroid cancer progression by inducing ferroptosis through m6A-TIAM1–Nrf2/HO-1 axis, suggesting ALKBH5 might be a potential target molecule for the treatment and diagnosis of thyroid cancer.
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         Nrf2/HO-1 pathway
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         Cancer Research
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