KLF5转录因子抑制TRAIL诱导PC-3前列腺癌细胞凋亡的分子机制

Chao Yang; Qi Shi; Jian Bin Ma; Peng Guo; Da Lin He

doi:10.7652/jdyxb202002010

KLF5转录因子抑制TRAIL诱导PC-3前列腺癌细胞凋亡的分子机制

Translated title of the contribution: KLF5 suppresses TRAIL-induced cell apoptosis in PC-3 prostate cancer cells

Chao Yang
, Qi Shi
, Jian Bin Ma
, Peng Guo
, Da Lin He

The First Affiliated Hospital of Xi’an Jiaotong University

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

Abstract

Objective： To explore the possibility of promoting tumor necrosis factor-related apoptosis inducing ligand (TRAIL)-induced apoptosis in prostate cancer PC-3 cell by inhibiting Krüppel-like factor 5 (KLF5). Methods： MTT assay, flow cytometry, Western blot assay and qRT-PCR assay were deployed to detect the cell viability, apoptosis and apoptotic markers in KLF5-inhibited and TRAIL-induced PC-3 cells. Results： After KLF5 was inhibited in TRAIL-induced PC-3 cells, cell viability reduced, apoptosis enhanced, the expressions of DR4 and DR5 increased while the expression of cellular fas-associated death domain-like interleukin-1β converting enzyme inhibitory protein (c-FLIP) decreased. Conclusion： Inhibiting KLF5 suppresses cell viability by promoting TRAIL-induced apoptosis in prostate cancer cell PC-3. It may be a potential means to treat hormone-insensitive prostate cancer.

Translated title of the contribution	KLF5 suppresses TRAIL-induced cell apoptosis in PC-3 prostate cancer cells
Original language	Chinese (Traditional)
Pages (from-to)	206-209
Number of pages	4
Journal	Journal of Xi'an Jiaotong University (Medical Sciences)
Volume	41
Issue number	2
DOIs	https://doi.org/10.7652/jdyxb202002010
State	Published - 5 Mar 2020
Externally published	Yes

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@article{07f4702e085646f09f83bba7fcb7e86a,

title = "KLF5转录因子抑制TRAIL诱导PC-3前列腺癌细胞凋亡的分子机制",

abstract = "Objective： To explore the possibility of promoting tumor necrosis factor-related apoptosis inducing ligand (TRAIL)-induced apoptosis in prostate cancer PC-3 cell by inhibiting Kr{\"u}ppel-like factor 5 (KLF5). Methods： MTT assay, flow cytometry, Western blot assay and qRT-PCR assay were deployed to detect the cell viability, apoptosis and apoptotic markers in KLF5-inhibited and TRAIL-induced PC-3 cells. Results： After KLF5 was inhibited in TRAIL-induced PC-3 cells, cell viability reduced, apoptosis enhanced, the expressions of DR4 and DR5 increased while the expression of cellular fas-associated death domain-like interleukin-1β converting enzyme inhibitory protein (c-FLIP) decreased. Conclusion： Inhibiting KLF5 suppresses cell viability by promoting TRAIL-induced apoptosis in prostate cancer cell PC-3. It may be a potential means to treat hormone-insensitive prostate cancer.",

keywords = "Apoptosis, Cellular fas-associated death domain-like interleukin-1β converting enzyme inhibitory protein (c-FLIP), Kr{\"u}ppel-like factor 5 (KLF5), Prostate cancer, Tumor necrosis factor-related apoptosis inducing ligand (TRAIL)",

author = "Chao Yang and Qi Shi and Ma, \{Jian Bin\} and Peng Guo and He, \{Da Lin\}",

year = "2020",

month = mar,

day = "5",

doi = "10.7652/jdyxb202002010",

language = "繁体中文",

volume = "41",

pages = "206--209",

journal = "Journal of Xi'an Jiaotong University (Medical Sciences)",

issn = "1671-8259",

publisher = "Xi'an Medical University",

number = "2",

}

TY - JOUR

T1 - KLF5转录因子抑制TRAIL诱导PC-3前列腺癌细胞凋亡的分子机制

AU - Yang, Chao

AU - Shi, Qi

AU - Ma, Jian Bin

AU - Guo, Peng

AU - He, Da Lin

PY - 2020/3/5

Y1 - 2020/3/5

N2 - Objective： To explore the possibility of promoting tumor necrosis factor-related apoptosis inducing ligand (TRAIL)-induced apoptosis in prostate cancer PC-3 cell by inhibiting Krüppel-like factor 5 (KLF5). Methods： MTT assay, flow cytometry, Western blot assay and qRT-PCR assay were deployed to detect the cell viability, apoptosis and apoptotic markers in KLF5-inhibited and TRAIL-induced PC-3 cells. Results： After KLF5 was inhibited in TRAIL-induced PC-3 cells, cell viability reduced, apoptosis enhanced, the expressions of DR4 and DR5 increased while the expression of cellular fas-associated death domain-like interleukin-1β converting enzyme inhibitory protein (c-FLIP) decreased. Conclusion： Inhibiting KLF5 suppresses cell viability by promoting TRAIL-induced apoptosis in prostate cancer cell PC-3. It may be a potential means to treat hormone-insensitive prostate cancer.

AB - Objective： To explore the possibility of promoting tumor necrosis factor-related apoptosis inducing ligand (TRAIL)-induced apoptosis in prostate cancer PC-3 cell by inhibiting Krüppel-like factor 5 (KLF5). Methods： MTT assay, flow cytometry, Western blot assay and qRT-PCR assay were deployed to detect the cell viability, apoptosis and apoptotic markers in KLF5-inhibited and TRAIL-induced PC-3 cells. Results： After KLF5 was inhibited in TRAIL-induced PC-3 cells, cell viability reduced, apoptosis enhanced, the expressions of DR4 and DR5 increased while the expression of cellular fas-associated death domain-like interleukin-1β converting enzyme inhibitory protein (c-FLIP) decreased. Conclusion： Inhibiting KLF5 suppresses cell viability by promoting TRAIL-induced apoptosis in prostate cancer cell PC-3. It may be a potential means to treat hormone-insensitive prostate cancer.

KW - Apoptosis

KW - Cellular fas-associated death domain-like interleukin-1β converting enzyme inhibitory protein (c-FLIP)

KW - Krüppel-like factor 5 (KLF5)

KW - Prostate cancer

KW - Tumor necrosis factor-related apoptosis inducing ligand (TRAIL)

UR - https://www.scopus.com/pages/publications/85081658617

U2 - 10.7652/jdyxb202002010

DO - 10.7652/jdyxb202002010

M3 - 文章

AN - SCOPUS:85081658617

SN - 1671-8259

VL - 41

SP - 206

EP - 209

JO - Journal of Xi'an Jiaotong University (Medical Sciences)

JF - Journal of Xi'an Jiaotong University (Medical Sciences)

IS - 2

ER -

KLF5转录因子抑制TRAIL诱导PC-3前列腺癌细胞凋亡的分子机制

Abstract

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