Evidence map›Paper›PMID 32142918›Full record

ArticleCancer letters2020

Drosha-independent miR-6778-5p strengthens gastric cancer stem cell stemness via regulation of cytosolic one-carbon folate metabolism.

Maojia Zhao, Yixuan Hou, Yan-E Du, Liping Yang, Yilu Qin, Meixi Peng, Shuiqing Liu, Xueying Wan, Yina Qiao, Huan Zeng and 3 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 37 citations in OpenAlex.

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  17. The Drosha-Independent MicroRNA6778-5p/GSK3Computational intelligence and neuroscience · 2022
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 2 countries.

Maojia ZhaoKey Laboratory of Laboratory Medical Diagnostics Designated By Chinese Ministry of Education, Chongqing Medical University, Chongqing, 400016, China.
Yixuan HouExperimental Teaching Center of Basic Medicine Science, Chongqing Medical University, Chongqing, 400016, China.
Yan-E DuDepartment of Laboratory Medicine, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Liping YangKey Laboratory of Laboratory Medical Diagnostics Designated By Chinese Ministry of Education, Chongqing Medical University, Chongqing, 400016, China.
Yilu QinKey Laboratory of Laboratory Medical Diagnostics Designated By Chinese Ministry of Education, Chongqing Medical University, Chongqing, 400016, China.
Meixi PengKey Laboratory of Laboratory Medical Diagnostics Designated By Chinese Ministry of Education, Chongqing Medical University, Chongqing, 400016, China.
Shuiqing LiuKey Laboratory of Laboratory Medical Diagnostics Designated By Chinese Ministry of Education, Chongqing Medical University, Chongqing, 400016, China.
Xueying WanKey Laboratory of Laboratory Medical Diagnostics Designated By Chinese Ministry of Education, Chongqing Medical University, Chongqing, 400016, China.
Yina QiaoKey Laboratory of Laboratory Medical Diagnostics Designated By Chinese Ministry of Education, Chongqing Medical University, Chongqing, 400016, China.
Huan ZengKey Laboratory of Laboratory Medical Diagnostics Designated By Chinese Ministry of Education, Chongqing Medical University, Chongqing, 400016, China.
Xiaojiang CuiDepartment of Surgery, Department of Obstetrics and Gynecology, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center. Los Angeles, CA, 91006, USA.
Yong TengDepartment of Oral Biology, Dental College of Georgia, Georgia Cancer Center, Augusta University, Augusta, GA, USA.
Manran LiuKey Laboratory of Laboratory Medical Diagnostics Designated By Chinese Ministry of Education, Chongqing Medical University, Chongqing, 400016, China. Electronic address: manranliu@cqmu.edu.cn.
Chongqing Medical University · CNAugusta University · USCedars-Sinai Medical Center · USDalian Medical University · CN

Funding

The Role of FOXCI in Basal-like Breast CancerR01CA151610 · NCI · SAINT JOHN'S CANCER INSTITUTE · PI CUI, XIAOJIANG · 2011 to 2022
$3.8M
NCI NIH HHS R01 CA151610
6 · The paper itself

Abstract

Drosha-dependent canonical microRNAs (miRNAs) play a crucial role in the biological functions and development of cancer. However, the effects of Drosha-independent non-canonical miRNAs remain poorly understood. In our previous work, we found a set of aberrant miRNAs, including some upregulated miRNAs, called Drosha-independent noncanonical miRNAs, in Drosha-knockdown gastric cancer (GC) cells. Surprisingly, Drosha-silenced GC cells still retained strong malignant properties (e.g., proliferation ability and cancer stem cell (CSC) characteristics), indicating that aberrantly upregulated non-canonical miRNAs may play an important role in the maintenance of the malignant properties in GC cells that express low Drosha levels. Here, we report that miR-6778-5p, a noncanonical miRNA, acts as a crucial regulator for maintenance of CSC stemness in Drosha-silenced GC cells. MiR-6778-5p belongs to the 5'-tail mirtron type of non-canonical miRNAs and is transcript splice-derived from intron 5 of SHMT1 (coding cytoplasmic serine hydroxymethyltransferase). It positively regulates expression of its host gene, SHMT1, via targeting YWHAE in Drosha-knockdown GC cells. Similar to its family member SHMT2, SHMT1 plays a crucial role in folate-dependent serine/glycine inter-conversion in one-carbon metabolism. In Drosha wild type GC cells, SHMT2 mediates a mitochondrial-carbon metabolic pathway, which is a major pathway of one-carbon metabolism in normal cells and most cancer cells. However, in Drosha-silenced or Drosha low-expressing GC cells, miR-6778-5p positively regulates SHMT1, instead of SHMT2, thus mediating a compensatory activation of cytoplasmic carbon metabolism that plays an essential role in the maintenance of CSCs in gastric cancer (GCSCs). Drosha wild type GCSCs with SHMT2 are sensitive to 5-fluorouracil; however, Drosha low-expressing GCSCs with SHMT1 are 5-FU-resistant. The loss of miR-6778-5p or SHMT1 notably mitigates GCSC sphere formation and increases sensitivity to 5-fluorouracil in Drosha-knockdown gastric cancer cells. Thus, our study reveals a novel function of Drosha-independent noncanonical miRNAs in maintaining the stemness of GCSCs.

Indexed as

14-3-3 ProteinsAnimalsCarbonCell Line, TumorCytosolFemaleFluorouracilFolic AcidGene Expression Regulation, NeoplasticGlycine HydroxymethyltransferaseHumansMiceMicroRNAsNeoplasm TransplantationNeoplastic Stem CellsRibonuclease III14-3-3 ProteinsCarbonDROSHA protein, humanFluorouracilFolic AcidGlycine HydroxymethyltransferaseMicroRNAsRibonuclease IIISHMT protein, humanYWHAE protein, humanCytoplasmic serine hydroxyl methyltransferaseDrosha-independent miRNAGastric CSCmiR-6778–5pOne-carbon metabolism

Identifiers

PMID32142918
PMCPMC7474538
OpenAlexW3009702734

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.