Deep sequencing of transcriptome profiling of GSTM2 knock-down in swine testis cells

Lv, Yuqi; Jin, Y.; Zhou, Yongqiang; Jin, Jianjun; Ma, Zhenfa; Ren, Zhuqing

doi:10.1038/srep38254

Cited by 9 publications

(7 citation statements)

References 63 publications

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“…Western blotting was performed as reported previously [58]. Briefly, cells were collected and homogenized in lysis buffer (#P0013, Beyotime Biotechnology, Nanjing, China).…”

Section: Methodsmentioning

confidence: 99%

Perilipin 5 Protects against Cellular Oxidative Stress by Enhancing Mitochondrial Function in HepG2 Cells

Tan

Jin

Wang

et al. 2019

Cells

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Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases worldwide. Reactive oxygen species (ROS), as potent oxidants in cells, have been shown to promote the development of NAFLD. Previous studies reported that for ROS-induced cellular oxidative stress, promoting lipid droplet (LD) accumulation is associated with the cellular antioxidation process. However, the regulatory role of LDs in relieving cellular oxidative stress is poorly understood. Here, we showed that Perilipin 5 (PLIN5), a key LD protein related to mitochondria–LD contact, reduced ROS levels and improved mitochondrial function in HepG2 cells. Both mRNA and protein levels of PLIN5 were significantly increased in cells with hydrogen peroxide or lipopolysaccharide (LPS) treatment (p < 0.05). Additionally, the overexpression of PLIN5 promoted LD formation and mitochondria–LD contact, reduced cellular ROS levels and up-regulated mitochondrial function-related genes such as COX and CS. Knockdown PLIN5, meanwhile, showed opposite effects. Furthermore, we identified that cellular oxidative stress up-regulated PLIN5 expression via the JNK-p38-ATF pathway. This study shows that the up-regulation of PLIN5 is a kind of survival strategy for cells in response to stress. PLIN5 can be a potential therapeutic target in NAFLD.

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“…Western blotting was performed as reported previously [58]. Briefly, cells were collected and homogenized in lysis buffer (#P0013, Beyotime Biotechnology, Nanjing, China).…”

Section: Methodsmentioning

confidence: 99%

Perilipin 5 Protects against Cellular Oxidative Stress by Enhancing Mitochondrial Function in HepG2 Cells

Tan

Jin

Wang

et al. 2019

Cells

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“…Western blotting was performed as reported previously [51]. The following antibodies were used: anti- PSMD1 (#A16420; rabbit polyclonal antibody; ABclonal; 1:1000 dilution), anti- PSMD2 (#14748-1-AP; rabbit polyclonal antibody; Proteintech; 1:1000 dilution), anti-ASK1 (#A6274; rabbit polyclonal antibody; ABclonal; 1:2000 dilution), anti- p-ASK1 (#AP0394; rabbit polyclonal antibody; ABclonal; 1:2000 dilution), anti-AKT (#A11027; rabbit polyclonal antibody; ABclonal; 1:2000 dilution), anti-p-AKT (#AP0140; rabbit polyclonal antibody; ABclonal; 1:2000 dilution), anti-p38 (#A10832; rabbit polyclonal antibody; ABclonal; 1:2000 dilution), anti-p-p38 (#AP0297; rabbit polyclonal antibody; ABclonal; 1:2000 dilution), anti-JNK1/2 (#A11119; rabbit polyclonal antibody; ABclonal; 1:2000 dilution), anti-p-JNK1/2 (#AP0631; rabbit polyclonal antibody; ABclonal; 1:2000 dilution), anti-GAPDH (Servicebio, Wuhan, China; 1:2000 dilution), anti-Tubulin (Servicebio, Wuhan, China; 1:2000 dilution), HRP-labeled Goat Anti-Rabbit IgG (H + L) (#GB23303-1, Servicebio, Wuhan, China), and HRP-labeled Goat Anti-Mouse IgG (H + L) (#GB23301, Servicebio, Wuhan, China).…”

Section: Methodsmentioning

confidence: 99%

PSMD1 and PSMD2 regulate HepG2 cell proliferation and apoptosis via modulating cellular lipid droplet metabolism

Tan

Jin

et al. 2019

BMC Molecular Biol

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BackgroundObesity and nonalcoholic steatohepatitis (NASH) are well-known risk factors of hepatocellular carcinoma (HCC). The lipid-rich environment enhances the proliferation and metastasis abilities of tumor cells. Previous studies showed the effect of the ubiquitin–proteasome system (UPS) on tumor cell proliferation. However, the underlying mechanism of UPS in regulating the proliferation of lipid-rich tumor cells is not totally clear.ResultsHere, we identify two proteasome 26S subunits, non-ATPase 1 and 2 (PSMD1 and PSMD2), which regulate HepG2 cells proliferation via modulating cellular lipid metabolism. Briefly, the knockdown of PSMD1 and/or PSMD2 decreases the formation of cellular lipid droplets, the provider of the energy and membrane components for tumor cell proliferation. Mechanically, PSMD1 and PSMD2 regulate the expression of genes related to de novo lipid synthesis via p38-JNK and AKT signaling. Moreover, the high expression of PSMD1 and PSMD2 is significantly correlated with poor prognosis of HCC.ConclusionWe demonstrate that PSMD1 and PSMD2 promote the proliferation of HepG2 cells via facilitating cellular lipid droplet accumulation. This study provides a potential therapeutic strategy for the treatment of lipid-rich tumors.

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“…The median age of the patients was 49 years, (range, 31–59 years). The number of patients in each staging was as follows: Stage Ib ( 10 ), stage IIa ( 12 ), stage IIb ( 5 ). None of the patients received preoperative adjuvant radiotherapy or chemotherapy.…”

Section: Methodsmentioning

confidence: 99%

“…Upon treatment, mRNA was isolated using Oligo d(T)25 Magnetic Beads (New England Biolabs, Inc., Ipswich, MA, USA). RNA preparation was performed as previously described ( 12 ). The mRNA was digested into short fragments and cDNA was synthesized using the mRNA fragments as templates.…”

Section: Methodsmentioning

confidence: 99%

Transcriptome profiling of cancer and normal tissues from cervical squamous cancer patients by deep sequencing

Lin

Feng

et al. 2017

Molecular Medicine Reports

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Cervical cancer is the fourth leading cause of cancer mortality in women worldwide. High-risk human papillomavirus infection is a major cause of cervical cancer. A previous study revealed the role of different oncogenes and tumor suppressors in cervical cancer initiation and progression. However, the complicated genetic network regulating cervical cancer remains largely unknown. The present study reported transcriptome sequencing analysis of three cervical squamous cell cancer tissues and paired normal cervical tissues. Transcriptomic analysis revealed that 2,519 genes were differently expressed between cervical cancer tissues and their corresponding normal tissues. Among these, 236 differentially expressed genes (DEGs) were statistically significant, including many DEGs that were novel in cervical cancer, including gastrulation brain homeobox 2,5-hydroxytryptamine receptor 1D and endothelin 3. These 236 significant DEGs were highly enriched in 28 functional gene ontology categories. The Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis suggested involvement of these DEGs in multiple pathways. The present study provides a transcriptome landscape of cervical cancer in Chinese patients and an improved understanding of the genetic regulatory network in cervical cancer tumorigenesis.

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Deep sequencing of transcriptome profiling of GSTM2 knock-down in swine testis cells

Cited by 9 publications

References 63 publications

Perilipin 5 Protects against Cellular Oxidative Stress by Enhancing Mitochondrial Function in HepG2 Cells

Perilipin 5 Protects against Cellular Oxidative Stress by Enhancing Mitochondrial Function in HepG2 Cells

PSMD1 and PSMD2 regulate HepG2 cell proliferation and apoptosis via modulating cellular lipid droplet metabolism

Transcriptome profiling of cancer and normal tissues from cervical squamous cancer patients by deep sequencing

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