STAT3 regulated ATR via microRNA-383 to control DNA damage to affect apoptosis in A431 cells

Liao, Xing–Hua; Li, Zheng; He, Hongbin; Zheng, De-Liang; Wei, Zhaoqiang; Wang, Nan; Dong, Jian; Ma, Wenjian; Zhang, Tongcun

doi:10.1016/j.cellsig.2015.08.005

Cited by 41 publications

(32 citation statements)

References 39 publications

(43 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…18 Results of a study showed that exposure to UV led to a significantly lower expression of miR-383 in A431cells (a model human cell line of epidermoid carcinoma). 19 In contrast to the results of the above study, in another study, overexpression of miR-383 inhibited ESCC cell proliferation in vitro and in vivo. 20 However, its expression pattern, clinical relevance, and functional role in CRC still remain unknown.…”

Section: Introductioncontrasting

confidence: 40%

“…5 Therefore, knowing more about the biology and nature of colorectal cancer, it is possible to design effective prognostic, diagnostic, and treatment plans to help reduce the rate of this disease. 6 MicroRNAs (miRNAs) are a class of small (18)(19)(20)(21)(22)(23)(24) noncoding RNAs that regulate gene expression at post translation levels. 7,8 This molecular RNAs regulate many biological processes.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Prognostic and predictive roles of microRNA-383 in colorectal cancer

Fateh

Feizi

Safaralizadeh

et al. 2016

Gastroenterol Insights

View full text Add to dashboard Cite

MicroRNAs (miRNAs) are impressive regulators of gene expression that have a critical role in the pathogenesis of colorectal cancer (CRC). With respect to the aberrant expression of miRNA-383 (miR-383) in some types of human malignancy, this prospective study characterized its contribution to CRC tumorigenesis. The real-time reverse transcriptionpolymerase chain reaction was used to examine miR-383 expression levels prospectively in 40 sample pairs of CRC tissues and adjacent noncancerous tissues (>2 cm from cancer tissue). No significant relationship was found between miR-383 expression levels and clinicopathological features. The ability of miR-383 to function as a tumor marker was also examined. Showing significant changes overall, miR-383 expression levels were significantly down regulated in the group of CRC samples compared with matched noncancerous tissue samples. A receiver-operating characteristic (ROC) curve also showed ROC area of 70% for miR-383 with 68 and 75% sensitivity and specificity, respectively. Therefore, miR-383 can be considered as a tumor marker in CRC and help as a potential predictive biomarker in the diagnosis of colorectal cancer.

show abstract

Section: Introductioncontrasting

confidence: 40%

Section: Introductionmentioning

confidence: 99%

Prognostic and predictive roles of microRNA-383 in colorectal cancer

Fateh

Feizi

Safaralizadeh

et al. 2016

Gastroenterol Insights

View full text Add to dashboard Cite

show abstract

“…We demonstrated that miR-520d-5p expression was reduced following IL6 treatment and that silencing STAT3 could abrogate this reduction. Recent studies have identified several tumor miRNAs that can be repressed by STAT3 (25,26,44), possibly by recruiting the corepressor complex under the regulation of specific cellular contexts or chromatin features, indicating a potential role for STAT3 in regulating miRNA networks. Furthermore, we also predicted multiple potential binding sites within the miR-520d promoter.…”

Section: Discussionmentioning

confidence: 99%

Gastric Cancer Cell Proliferation and Survival Is Enabled by a Cyclophilin B/STAT3/miR-520d-5p Signaling Feedback Loop

Guo

Zhao

et al. 2017

Cancer Research

View full text Add to dashboard Cite

Molecular links between inflammation and cancer remain obscure despite their great pathogenic significance. The JAK2/ STAT3 pathway activated by IL6 and other proinflammatory cytokines has garnered attention as a pivotal link in cancer pathogenesis, but the basis for its activation in cancer cells is not understood. Here we report that an IL6-triggered feedback loop involving STAT3-mediated suppression of miR-520d-5p and upregulation of its downstream target cyclophilin B (CypB) regulate the growth and survival of gastric cancer cells. In clinical specimens of gastric cancer, we documented increased expression of CypB and activation of STAT3. Mechanistic investigations identified miR-520d-5p as a regulator of CypB mRNA levels. This signaling axis regulated gastric cancer growth by modulating phosphorylation of STAT3. Furthermore, miR-520d-5p was identified as a direct STAT3 target and IL6-mediated inhibition of miR-520d-5p relied upon STAT3 activity. Our findings define a positive feedback loop that drives gastric carcinogenesis as influenced by H. pylori infections that involve proinflammatory IL6 stimulation. Cancer Res; 77(5);

show abstract

“…In HCC, STAT3 is constitutively activated, which promotes human cervical cancer progression and poor prognosis (18,19). Notably, STAT3 is also involved in the overexpression of COX-2 in HCC (17).…”

Section: Introductionmentioning

confidence: 99%

“…STAT3 has been most closely associated with tumorigenesis (13,14). Previous studies demonstrated that constitutive STAT3 activation was frequently detected in numerous human cancers in vitro and in vivo (15)(16)(17). Furthermore, STAT3 participated in the physiological and pathological processes of HCC, including tumor cell survival, proliferation, angiogenesis and metastasis (13).…”

Section: Introductionmentioning

confidence: 99%