Journal: Breast Cancer Research : BCR

Article Title: Targeting interferon response genes sensitizes aromatase inhibitor resistant breast cancer cells to estrogen-induced cell death

doi: 10.1186/s13058-014-0506-7

Figure Lengend Snippet: STAT1/STAT2 knockdown reduces IFITM1 and PLSCR1 expression. (A and B) MCF-7:5C cells were transfected with sicontrol (siCon), STAT1 siRNA (siSTAT1) or STAT2 siRNA (siSTAT2) and STAT1, STAT2, IFITM1 and PLSCR1 protein levels were assessed at 24 and 48 hours by Western blot analysis (left panels). Transfected cells were also treated with E 2 for an additional 24 and 48 hours and the above mentioned proteins were also measured (a and b, left panels). (A, B) Cell proliferation was measured in siSTAT1-knockdown and STAT2-knockdown cells in the presence or absence of E 2 by cell titer blue assay (right panels). Each value is a mean ± SD from three experiments. * P <0.05 or ** P <0.01 versus the control; # P <0.05 versus E 2 treatment. (C) MCF-7:5C cells were transfected with Bax siRNA (siBax) or Noxa siRNA (siNoxa) for 24 hours and then treated with 1 nM E 2 for an additional 24, 48 or 72 hours. Cells were harvested and analyzed for Bax, PLSCR1, Noxa, and IFITM1 protein expression by Western blot. Membranes were stripped and reprobed for β-actin, which was used as a loading control. E 2 , 17β-estradiol; IFITM1, interferon induced transmembrane protein1; PLSCR1, phospholipid scramblase 1; SD, standard deviation; STAT1,2, Signal transducer and activator of transcription 1,2.

Article Snippet: The siPLSCR1 (cat# sc-44028), siIFITM1 (cat# sc-44549), siSTAT1 (cat# sc-44123), siSTAT2 (cat# sc-29492), siIFNα (cat# sc-63324), siIRF-7 (cat# 38011) and siRNA negative control (cat# sc-37007) were purchased from Santa Cruz Biotechnology, and siBax and siNoxa were purchased from Thermo Fisher Scientific (Pittsburg, PA, USA).

Techniques: Knockdown, Expressing, Transfection, Western Blot, Control, Standard Deviation

Journal: Amino Acids

Article Title: Escherichia coli infection activates the production of IFN-α and IFN-β via the JAK1/STAT1/2 signaling pathway in lung cells

doi: 10.1007/s00726-021-03077-6

Figure Lengend Snippet: The sequences of siRNAs used in the present study

Article Snippet: Small interfering RNAs (siRNAs) targeting JAK1, STAT1, and STAT2 were designed using the siDESIGN Center of Dharmacon, and they were synthesized by Biosyntech (Suzhou, China).

Techniques: Sequencing

Journal: Amino Acids

Article Title: Escherichia coli infection activates the production of IFN-α and IFN-β via the JAK1/STAT1/2 signaling pathway in lung cells

doi: 10.1007/s00726-021-03077-6

Figure Lengend Snippet: The sequences of primers used in the present study

Article Snippet: Small interfering RNAs (siRNAs) targeting JAK1, STAT1, and STAT2 were designed using the siDESIGN Center of Dharmacon, and they were synthesized by Biosyntech (Suzhou, China).

Techniques: Sequencing

Journal: Amino Acids

Article Title: Escherichia coli infection activates the production of IFN-α and IFN-β via the JAK1/STAT1/2 signaling pathway in lung cells

doi: 10.1007/s00726-021-03077-6

Figure Lengend Snippet: E. coli infections increased the expression levels of the main components of the JAK1/STAT signaling pathway in lung cells. A E. coli infections (55 × 104 and 1 × 105 CFU, 24 h) significantly increased mRNA expression of JAK1 in the BEAS-2B cell line ( n = 4, * P < 0.05); B E. coli infections (5 × 104 and 1 × 105 CFU, 24 h) remarkably increased the mRNA levels of STAT1 in the BEAS-2B cell line ( n = 4, * P < 0.05); C E. coli infections (5 × 104 and 1 × 105 CFU, 24 h) remarkably increased the mRNA levels of STAT2 ( n = 4, * P < 0.05, ** P < 0.01); D E. coli infections (5 × 104 and 1 × 105 CFU, 24 h) significantly increased the mRNA levels of JAK1 in the HFL1 cell line ( n = 4, * P < 0.05, ** P < 0.01); E E. coli infections (5 × 104 and 1 × 105 CFU, 24 h) significantly increased the mRNA levels of STAT1 in the HFL1 cell line ( n = 4, * P < 0.05); F E. coli infections (5 × 104 and 1 × 105 CFU, 24 h) significantly increased the mRNA levels of STAT2 in the HFL1 cell line ( n = 4, * P < 0.05). G E. coli infection (5 × 104 CFU) increased phosphorylation level of JAK1, STAT1, and STAT1 in BEAS-2B cell line over time (24 and 48 h). H E. coli infection (5 × 104 CFU) increased phosphorylation level of JAK1, STAT1, and STAT1 in HFL1 cell line over time (24 and 48 h)

Article Snippet: Small interfering RNAs (siRNAs) targeting JAK1, STAT1, and STAT2 were designed using the siDESIGN Center of Dharmacon, and they were synthesized by Biosyntech (Suzhou, China).

Techniques: Expressing, Infection, Phospho-proteomics

Journal: Amino Acids

Article Title: Escherichia coli infection activates the production of IFN-α and IFN-β via the JAK1/STAT1/2 signaling pathway in lung cells

doi: 10.1007/s00726-021-03077-6

Figure Lengend Snippet: STAT2 knockdown compromised the E. coli infection-mediated enhancement of the expression levels of IFN-α and IFN-β in lung cells. A STAT2 was successfully knocked down in the BEAS-2B cell line, as shown using qPCR assays ( n = 4, ** P < 0.01); B STAT2 was successfully knocked down in the HFL1 cell line, as shown using qPCR assays ( n = 4, ** P < 0.01); C STAT2 was successfully knocked down in the BEAS-2B cell line, as shown using WB assays; D STAT2 was successfully knocked down in the HFL1 cell line, as shown using WB assays; E STAT2 knockdown could abolish the E. coli infection (1 × 105 CFU, 24 h)-mediated enhancement of the expression level of IFN-α in the BEAS-2B cell line ( n = 4, ** P < 0.01); F STAT2 knockdown could abolish the E. coli infection (1 × 105 CFU, 24 h)-mediated enhancement of the expression level of IFN-β in the BEAS-2B cell line ( n = 4, * P < 0.05, ** P < 0.01); G STAT2 knockdown could abolish the E. coli infection (1 × 105 CFU, 24 h)-mediated enhancement of the expression level of IFN-α in the HFL1 cell line ( n = 4, ** P < 0.01); (H) STAT2 knockdown could abolish the E. coli infection (1 × 105 CFU, 24 h)-mediated enhancement of the expression level of IFN-β in the HFL1 cell line ( n = 4, * P < 0.05)

Article Snippet: Small interfering RNAs (siRNAs) targeting JAK1, STAT1, and STAT2 were designed using the siDESIGN Center of Dharmacon, and they were synthesized by Biosyntech (Suzhou, China).

Techniques: Knockdown, Infection, Expressing

Journal: Amino Acids

Article Title: Escherichia coli infection activates the production of IFN-α and IFN-β via the JAK1/STAT1/2 signaling pathway in lung cells

doi: 10.1007/s00726-021-03077-6

Figure Lengend Snippet: Silencing JAK1, STAT1, and STAT2 abolished the E. coli infection-mediated promotion of the expression level of ISGs in lung cells. A JAK1 knockdown abolished the E. coli -mediated promotion of ISGs including ISG20, MX1, and IFIT1 in the BEAS-2B cell line ( n = 4, ** P < 0.01) B STAT1 knockdown abolished the E. coli -mediated promotion of ISGs including ISG20, MX1, and IFIT1 in the BEAS-2B cell line ( n = 4, * P < 0.05, ** P < 0.01); C STAT2 knockdown abolished the E. coli -mediated promotion of ISGs including ISG20, MX1, and IFIT1 in the BEAS-2B cell line ( n = 4, ** P < 0.01); D the knockdown of JAK1 abolished the E. coli -mediated promotion (1 × 105 CFU, 24 h) of ISGs including ISG20, MX1, and IFIT1 in the HFL1 cell line ( n = 4, * P < 0.05, ** P < 0.01); E the knockdown of STAT1 abolished the E. coli -mediated promotion (1 × 105 CFU, 24 h) of ISGs including ISG20, MX1, and IFIT1 in the HFL1 cell line ( n = 4, * P < 0.05, ** P < 0.01); F the knockdown of STAT2 abolished the E. coli -mediated promotion (1 × 105 CFU, 24 h) of ISGs including ISG20, MX1, and IFIT1 in the HFL1 cell line ( n = 4, * P < 0.05, ** P < 0.01)

Article Snippet: Small interfering RNAs (siRNAs) targeting JAK1, STAT1, and STAT2 were designed using the siDESIGN Center of Dharmacon, and they were synthesized by Biosyntech (Suzhou, China).

Techniques: Infection, Expressing, Knockdown