ArticleExperimental and therapeutic medicine2016
Expression and functions of the STAT3-SCLIP pathway in chronic myeloid leukemia cells.
Article in Experimental and therapeutic medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Mechanisms and therapeutic potential of glycyrrhizic acid: Insights into key signaling pathways and disease modulation (Review).Molecular medicine reports · 2026Review
- Beyond STMN1: stathmin-family control of microtubule dynamics and paclitaxel resistance in cancer.Frontiers in oncology · 2026Review
- FAM168A participates in the development of chronic myeloid leukemia via BCR-ABL1/AKT1/NFκB pathway.BMC cancer · 2019Article
- Using glycyrrhizic acid to target sumoylation processes during Epstein-Barr virus latency.PloS one · 2019Article
- The roles of STMN3 in various cancers.Science progressReview
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic myeloid leukemia (CML) is a blood cell cancer with increased proliferation of granulocytes. Signal transducers and activators of transcription 3 (STAT3) is an important regulator of CML. To investigate the possible downstream factors of STAT3 and gain more insight into CML-related pathways, this study focused on the superior cervical ganglia protein 10-like protein (SCLIP, or SCG 10-like protein) and analyzed the functions of the STAT3-SCLIP pathway. The effects of STAT3 phosphorylation on SCLIP expression were examined by western blotting. Specific small interfering RNA (siRNA) was then used to knockdown SCLIP in the CML cell line K562 and the expression changes of STAT3 and factors further downstream, namely Bcl-2 and cyclin E1, were detected by RT-qPCR. Cell viability and apoptosis were also analyzed following the knockdown of SCLIP. Results showed a positive association between the phosphorylation of STAT3 and the expression of SCLIP. Knockdown of SCLIP inhibited the viability and induced the apoptosis of K562 cells. Knockdown of SCLIP did not affect the expression of
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Registered trials
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