RETRACTED ARTICLE: ALKBH5 inhibits thyroid cancer progression by promoting ferroptosis through TIAM1–Nrf2/HO-1 axis

Sep 7, 2022Molecular and cellular biochemistry

ALKBH5 may slow thyroid cancer growth by encouraging cell death through the TIAM1-controlled antioxidant pathway

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Abstract

ALKBH5 was decreased in thyroid cancer tissues and cells.

Overexpression of ALKBH5 inhibited thyroid cancer cell proliferation.
Increased levels of iron and reactive oxygen species (ROS) were observed with ALKBH5 overexpression.
ALKBH5 reduced the expression of proteins GPX4 and SLC7A11.
ALKBH5 overexpression inhibited TIAM1 expression through m6A modification.
TIAM1 was found to be elevated in thyroid cancer, and its knockdown decreased cell proliferation and promoted ferroptosis.
In vivo studies indicated that ALKBH5 suppressed thyroid cancer progression by reducing the m6A level of TIAM1.

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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 Feand 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. 2+

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RETRACTED ARTICLE: ALKBH5 inhibits thyroid cancer progression by promoting ferroptosis through TIAM1–Nrf2/HO-1 axis

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