Long noncoding RNA SNHG16 contributes to the development of bladder cancer via regulating miR‐98/STAT3/Wnt/β‐catenin pathway axis

This study aimed to investigate the role and the possible mechanism of the long noncoding small nucleolar RNA host gene 16 (SNHG16) in bladder cancer development. The expression of SNHG16 in the tumor tissues and plasma of patients with bladder cancer as well as bladder cancer cell lines was detecte...

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Published in:Journal of cellular biochemistry Vol. 119; no. 11; pp. 9408 - 9418
Main Authors: Feng, Feng, Chen, Aiping, Huang, Junjian, Xia, Qinghua, Chen, Yougen, Jin, Xunbo
Format: Journal Article
Language:English
Published: United States 01.11.2018
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ISSN:0730-2312, 1097-4644, 1097-4644
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Abstract This study aimed to investigate the role and the possible mechanism of the long noncoding small nucleolar RNA host gene 16 (SNHG16) in bladder cancer development. The expression of SNHG16 in the tumor tissues and plasma of patients with bladder cancer as well as bladder cancer cell lines was detected. T24 cells were then transfected with sh‐SNHG16 to further investigate the effects of suppression of SNHG16 on T24 cell proliferation, apoptosis, migration, and invasion. In addition, the regulatory relationships between SNHG16 and miR‐98 as well as the target of miR‐98 were explored. Besides, the association between SNHG16 and the Wnt/β‐catenin pathway was further elucidated. The SNHG16 expression was upregulated in the tumor tissues and plasma of patients with bladder cancer, as well as bladder cancer cells. Suppression of SNHG16 inhibited T24 cell proliferation, promoted apoptosis, and suppressed migration and invasion in vitro. In addition, SNHG16 negatively regulated miR‐98 expression and regulated the malignant behaviors of T24 cells through sponging miR‐98. Moreover, signal transducer and activator of transcription 3 (STAT3) was identified as a functional target of miR‐98, and miR‐98 regulated the malignant behaviors of bladder cancer cells by targeting STAT3. Besides, suppression of SNHG16 inhibited the activation of the Wnt/β‐catenin pathway, which was further regulated by miR‐98 and STAT3, indicating that the effects of SNHG16/miR‐98/STAT3 on T24 cells were achieved through the Wnt/β‐catenin pathway. Our findings reveal that long noncoding RNAs SNHG16 is upregulated in bladder cancer and contributes to the development of bladder cancer possibly via regulating the miR‐98/STAT3/Wnt/β‐catenin pathway axis. The SNHG16/miR‐98/STAT3/Wnt/β‐catenin pathway axis may provide a new strategy for bladder cancer treatment. Our research revealed that the long noncoding RNA (lncRNA) SNHG16 is upregulated in bladder cancer and contributes to the development of bladder cancer possibly via regulating the miR‐98/STAT3/Wnt/β‐catenin pathway axis. The SNHG16/miR‐98/STAT3/Wnt/β‐catenin pathway axis may provide a new strategy for bladder cancer treatment.
AbstractList This study aimed to investigate the role and the possible mechanism of the long noncoding small nucleolar RNA host gene 16 (SNHG16) in bladder cancer development. The expression of SNHG16 in the tumor tissues and plasma of patients with bladder cancer as well as bladder cancer cell lines was detected. T24 cells were then transfected with sh-SNHG16 to further investigate the effects of suppression of SNHG16 on T24 cell proliferation, apoptosis, migration, and invasion. In addition, the regulatory relationships between SNHG16 and miR-98 as well as the target of miR-98 were explored. Besides, the association between SNHG16 and the Wnt/β-catenin pathway was further elucidated. The SNHG16 expression was upregulated in the tumor tissues and plasma of patients with bladder cancer, as well as bladder cancer cells. Suppression of SNHG16 inhibited T24 cell proliferation, promoted apoptosis, and suppressed migration and invasion in vitro. In addition, SNHG16 negatively regulated miR-98 expression and regulated the malignant behaviors of T24 cells through sponging miR-98. Moreover, signal transducer and activator of transcription 3 (STAT3) was identified as a functional target of miR-98, and miR-98 regulated the malignant behaviors of bladder cancer cells by targeting STAT3. Besides, suppression of SNHG16 inhibited the activation of the Wnt/β-catenin pathway, which was further regulated by miR-98 and STAT3, indicating that the effects of SNHG16/miR-98/STAT3 on T24 cells were achieved through the Wnt/β-catenin pathway. Our findings reveal that long noncoding RNAs SNHG16 is upregulated in bladder cancer and contributes to the development of bladder cancer possibly via regulating the miR-98/STAT3/Wnt/β-catenin pathway axis. The SNHG16/miR-98/STAT3/Wnt/β-catenin pathway axis may provide a new strategy for bladder cancer treatment.
This study aimed to investigate the role and the possible mechanism of the long noncoding small nucleolar RNA host gene 16 (SNHG16) in bladder cancer development. The expression of SNHG16 in the tumor tissues and plasma of patients with bladder cancer as well as bladder cancer cell lines was detected. T24 cells were then transfected with sh‐SNHG16 to further investigate the effects of suppression of SNHG16 on T24 cell proliferation, apoptosis, migration, and invasion. In addition, the regulatory relationships between SNHG16 and miR‐98 as well as the target of miR‐98 were explored. Besides, the association between SNHG16 and the Wnt/β‐catenin pathway was further elucidated. The SNHG16 expression was upregulated in the tumor tissues and plasma of patients with bladder cancer, as well as bladder cancer cells. Suppression of SNHG16 inhibited T24 cell proliferation, promoted apoptosis, and suppressed migration and invasion in vitro. In addition, SNHG16 negatively regulated miR‐98 expression and regulated the malignant behaviors of T24 cells through sponging miR‐98. Moreover, signal transducer and activator of transcription 3 (STAT3) was identified as a functional target of miR‐98, and miR‐98 regulated the malignant behaviors of bladder cancer cells by targeting STAT3. Besides, suppression of SNHG16 inhibited the activation of the Wnt/β‐catenin pathway, which was further regulated by miR‐98 and STAT3, indicating that the effects of SNHG16/miR‐98/STAT3 on T24 cells were achieved through the Wnt/β‐catenin pathway. Our findings reveal that long noncoding RNAs SNHG16 is upregulated in bladder cancer and contributes to the development of bladder cancer possibly via regulating the miR‐98/STAT3/Wnt/β‐catenin pathway axis. The SNHG16/miR‐98/STAT3/Wnt/β‐catenin pathway axis may provide a new strategy for bladder cancer treatment. Our research revealed that the long noncoding RNA (lncRNA) SNHG16 is upregulated in bladder cancer and contributes to the development of bladder cancer possibly via regulating the miR‐98/STAT3/Wnt/β‐catenin pathway axis. The SNHG16/miR‐98/STAT3/Wnt/β‐catenin pathway axis may provide a new strategy for bladder cancer treatment.
This study aimed to investigate the role and the possible mechanism of the long noncoding small nucleolar RNA host gene 16 (SNHG16) in bladder cancer development. The expression of SNHG16 in the tumor tissues and plasma of patients with bladder cancer as well as bladder cancer cell lines was detected. T24 cells were then transfected with sh-SNHG16 to further investigate the effects of suppression of SNHG16 on T24 cell proliferation, apoptosis, migration, and invasion. In addition, the regulatory relationships between SNHG16 and miR-98 as well as the target of miR-98 were explored. Besides, the association between SNHG16 and the Wnt/β-catenin pathway was further elucidated. The SNHG16 expression was upregulated in the tumor tissues and plasma of patients with bladder cancer, as well as bladder cancer cells. Suppression of SNHG16 inhibited T24 cell proliferation, promoted apoptosis, and suppressed migration and invasion in vitro. In addition, SNHG16 negatively regulated miR-98 expression and regulated the malignant behaviors of T24 cells through sponging miR-98. Moreover, signal transducer and activator of transcription 3 (STAT3) was identified as a functional target of miR-98, and miR-98 regulated the malignant behaviors of bladder cancer cells by targeting STAT3. Besides, suppression of SNHG16 inhibited the activation of the Wnt/β-catenin pathway, which was further regulated by miR-98 and STAT3, indicating that the effects of SNHG16/miR-98/STAT3 on T24 cells were achieved through the Wnt/β-catenin pathway. Our findings reveal that long noncoding RNAs SNHG16 is upregulated in bladder cancer and contributes to the development of bladder cancer possibly via regulating the miR-98/STAT3/Wnt/β-catenin pathway axis. The SNHG16/miR-98/STAT3/Wnt/β-catenin pathway axis may provide a new strategy for bladder cancer treatment.This study aimed to investigate the role and the possible mechanism of the long noncoding small nucleolar RNA host gene 16 (SNHG16) in bladder cancer development. The expression of SNHG16 in the tumor tissues and plasma of patients with bladder cancer as well as bladder cancer cell lines was detected. T24 cells were then transfected with sh-SNHG16 to further investigate the effects of suppression of SNHG16 on T24 cell proliferation, apoptosis, migration, and invasion. In addition, the regulatory relationships between SNHG16 and miR-98 as well as the target of miR-98 were explored. Besides, the association between SNHG16 and the Wnt/β-catenin pathway was further elucidated. The SNHG16 expression was upregulated in the tumor tissues and plasma of patients with bladder cancer, as well as bladder cancer cells. Suppression of SNHG16 inhibited T24 cell proliferation, promoted apoptosis, and suppressed migration and invasion in vitro. In addition, SNHG16 negatively regulated miR-98 expression and regulated the malignant behaviors of T24 cells through sponging miR-98. Moreover, signal transducer and activator of transcription 3 (STAT3) was identified as a functional target of miR-98, and miR-98 regulated the malignant behaviors of bladder cancer cells by targeting STAT3. Besides, suppression of SNHG16 inhibited the activation of the Wnt/β-catenin pathway, which was further regulated by miR-98 and STAT3, indicating that the effects of SNHG16/miR-98/STAT3 on T24 cells were achieved through the Wnt/β-catenin pathway. Our findings reveal that long noncoding RNAs SNHG16 is upregulated in bladder cancer and contributes to the development of bladder cancer possibly via regulating the miR-98/STAT3/Wnt/β-catenin pathway axis. The SNHG16/miR-98/STAT3/Wnt/β-catenin pathway axis may provide a new strategy for bladder cancer treatment.
Author Xia, Qinghua
Jin, Xunbo
Feng, Feng
Chen, Aiping
Chen, Yougen
Huang, Junjian
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Issue 11
Keywords long noncoding RNA (lncRNA)
Wnt/β-catenin pathway
miR-98
small nucleolar RNA host gene 16 (SNHG16)
bladder cancer
signal transducer and activator of transcription 3 (STAT3)
Language English
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Notes Feng Feng and Aiping Chen contributed equally to this study.
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Snippet This study aimed to investigate the role and the possible mechanism of the long noncoding small nucleolar RNA host gene 16 (SNHG16) in bladder cancer...
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SubjectTerms bladder cancer
long noncoding RNA (lncRNA)
miR‐98
signal transducer and activator of transcription 3 (STAT3)
small nucleolar RNA host gene 16 (SNHG16)
Wnt/β‐catenin pathway
Title Long noncoding RNA SNHG16 contributes to the development of bladder cancer via regulating miR‐98/STAT3/Wnt/β‐catenin pathway axis
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