Induction of miR-21-PDCD4 signaling by UVB in JB6 cells involves ROS-mediated MAPK pathways

Lichao Hou; Linda Bowman; Terence G. Meighan; Poyil Pratheeshkumar; Xianglin Shi; Min Ding

doi:10.1016/j.etp.2013.05.006

Induction of miR-21-PDCD4 signaling by UVB in JB6 cells involves ROS-mediated MAPK pathways

Lichao Hou, Linda Bowman, Terence G. Meighan, Poyil Pratheeshkumar, Xianglin Shi, Min Ding

Research output: Contribution to journal › Article › peer-review

14 Scopus citations

Abstract

Ultraviolet (UV) irradiation plays a major role in the development of human skin cancer. The present study examined the alterations of miR-21-PDCD4 signaling in a mouse epidermal cell line (JB6 P⁺) post exposure to UVB irradiation. The results showed that (1) UVB caused PDCD4 inhibition in JB6 cells; (2) exposure of cells to UVB caused a significant increase of miR-21, the upstream regulator of PDCD4, expression; (3) both inhibition of ERKs with U0126 and inhibition of p38 with SB203580 significantly reversed UVB-induced PDCD4 inhibition; (4) ROS scavenger, N-acetyl-l-cysteine reversed the inhibitory effect of UVB on PDCD4 expression. The above results suggested that UVB induced PDCD4 inhibition, which may be mediated through ROS, especially endogenous H₂O₂ and p38 and ERKs phosphorylation. Unraveling the complex mechanisms associated with these events may provide insights into the initiation and progression of UVB-induced carcinogenesis.

Original language	English
Pages (from-to)	1145-1148
Number of pages	4
Journal	Experimental and Toxicologic Pathology
Volume	65
Issue number	7-8
DOIs	https://doi.org/10.1016/j.etp.2013.05.006
State	Published - Nov 2013

Keywords

JB6 cell
MicroRNA-21
PDCD4
Reactive oxygen species
Ultraviolet light

ASJC Scopus subject areas

Pathology and Forensic Medicine
Toxicology
Cell Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.etp.2013.05.006

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title = "Induction of miR-21-PDCD4 signaling by UVB in JB6 cells involves ROS-mediated MAPK pathways",

abstract = "Ultraviolet (UV) irradiation plays a major role in the development of human skin cancer. The present study examined the alterations of miR-21-PDCD4 signaling in a mouse epidermal cell line (JB6 P+) post exposure to UVB irradiation. The results showed that (1) UVB caused PDCD4 inhibition in JB6 cells; (2) exposure of cells to UVB caused a significant increase of miR-21, the upstream regulator of PDCD4, expression; (3) both inhibition of ERKs with U0126 and inhibition of p38 with SB203580 significantly reversed UVB-induced PDCD4 inhibition; (4) ROS scavenger, N-acetyl-l-cysteine reversed the inhibitory effect of UVB on PDCD4 expression. The above results suggested that UVB induced PDCD4 inhibition, which may be mediated through ROS, especially endogenous H2O2 and p38 and ERKs phosphorylation. Unraveling the complex mechanisms associated with these events may provide insights into the initiation and progression of UVB-induced carcinogenesis.",

keywords = "JB6 cell, MicroRNA-21, PDCD4, Reactive oxygen species, Ultraviolet light",

author = "Lichao Hou and Linda Bowman and Meighan, {Terence G.} and Poyil Pratheeshkumar and Xianglin Shi and Min Ding",

year = "2013",

month = nov,

doi = "10.1016/j.etp.2013.05.006",

language = "English",

volume = "65",

pages = "1145--1148",

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T1 - Induction of miR-21-PDCD4 signaling by UVB in JB6 cells involves ROS-mediated MAPK pathways

AU - Hou, Lichao

AU - Bowman, Linda

AU - Meighan, Terence G.

AU - Pratheeshkumar, Poyil

AU - Shi, Xianglin

AU - Ding, Min

PY - 2013/11

Y1 - 2013/11

N2 - Ultraviolet (UV) irradiation plays a major role in the development of human skin cancer. The present study examined the alterations of miR-21-PDCD4 signaling in a mouse epidermal cell line (JB6 P+) post exposure to UVB irradiation. The results showed that (1) UVB caused PDCD4 inhibition in JB6 cells; (2) exposure of cells to UVB caused a significant increase of miR-21, the upstream regulator of PDCD4, expression; (3) both inhibition of ERKs with U0126 and inhibition of p38 with SB203580 significantly reversed UVB-induced PDCD4 inhibition; (4) ROS scavenger, N-acetyl-l-cysteine reversed the inhibitory effect of UVB on PDCD4 expression. The above results suggested that UVB induced PDCD4 inhibition, which may be mediated through ROS, especially endogenous H2O2 and p38 and ERKs phosphorylation. Unraveling the complex mechanisms associated with these events may provide insights into the initiation and progression of UVB-induced carcinogenesis.

AB - Ultraviolet (UV) irradiation plays a major role in the development of human skin cancer. The present study examined the alterations of miR-21-PDCD4 signaling in a mouse epidermal cell line (JB6 P+) post exposure to UVB irradiation. The results showed that (1) UVB caused PDCD4 inhibition in JB6 cells; (2) exposure of cells to UVB caused a significant increase of miR-21, the upstream regulator of PDCD4, expression; (3) both inhibition of ERKs with U0126 and inhibition of p38 with SB203580 significantly reversed UVB-induced PDCD4 inhibition; (4) ROS scavenger, N-acetyl-l-cysteine reversed the inhibitory effect of UVB on PDCD4 expression. The above results suggested that UVB induced PDCD4 inhibition, which may be mediated through ROS, especially endogenous H2O2 and p38 and ERKs phosphorylation. Unraveling the complex mechanisms associated with these events may provide insights into the initiation and progression of UVB-induced carcinogenesis.

KW - JB6 cell

KW - MicroRNA-21

KW - PDCD4

KW - Reactive oxygen species

KW - Ultraviolet light

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Induction of miR-21-PDCD4 signaling by UVB in JB6 cells involves ROS-mediated MAPK pathways

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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