Evidence map›Paper›PMID 35167417›Full record

ArticleCell cycle (Georgetown, Tex.)2022

CDK6 increases glycolysis and suppresses autophagy by mTORC1-HK2 pathway activation in cervical cancer cells.

Xiaoxi Zhang, Yunxia Sun, Siyao Cheng, Yanjing Yao, Xintao Hua, Yueyue Shi, Xiaoqin Jin, Jieli Pan, Miaofen G Hu, Pian Ying and 2 more

Open access · greenAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
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

12 authors at 2 institutions in 2 countries.

Xiaoxi ZhangAcademy of Chinese Medical Science, Zhejiang Chinese Medical University, Hangzhou, China.
Yunxia SunAcademy of Chinese Medical Science, Zhejiang Chinese Medical University, Hangzhou, China.
Siyao ChengSchool of Life Sciences, Zhejiang Chinese Medical University, China.
Yanjing YaoSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, China.
Xintao HuaAcademy of Chinese Medical Science, Zhejiang Chinese Medical University, Hangzhou, China.
Yueyue ShiSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, China.
Xiaoqin JinAcademy of Chinese Medical Science, Zhejiang Chinese Medical University, Hangzhou, China.
Jieli PanAcademy of Chinese Medical Science, Zhejiang Chinese Medical University, Hangzhou, China.
Miaofen G HuDepartment of Medicine, Division of Hematology Oncology, Tufts Medical Center, Boston, MA, USA.
Pian YingDepartment of Gynecology and Obstetrics, The First Affiliated Hospital of Zhejiang Chinese Medical University, China.
Xiaoli HouAcademy of Chinese Medical Science, Zhejiang Chinese Medical University, Hangzhou, China.
Daozong XiaSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, China.
Zhejiang Chinese Medical University · CNTufts Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cervical carcinoma is a leading malignant tumor among women worldwide, characterized by the dysregulation of cell cycle. Cyclin-dependent kinase 6 (CDK6) plays important roles in the cell cycle progression, cell differentiation, and tumorigenesis. However, the role of CDK6 in cervical cancer remains controversial. Here, we found that loss of CDK6 in cervical adenocarcinoma HeLa cell line inhibited cell proliferation but induced apoptosis as well as autophagy, accompanied by attenuated expression of mammalian target of rapamycin complex 1 (mTORC1) and hexokinase 2 (HK2), reduced glycolysis, and production of protein, nucleotide, and lipid. Similarly, we showed that CDK6 knockout inhibited the survival of CDK6-high CaSki but not CDK6-low SiHa cervical cancer cells by regulation of glycolysis and autophagy process. Collectively, our studies indicate that CDK6 is a critical regulator of human cervical cancer cells, especially with high CDK6 level, through its ability to regulate cellular apoptosis and metabolism. Thus, inhibition of CDK6 kinase activity could be a powerful therapeutic avenue used to treat cervical cancers.

Indexed as

Cyclin-Dependent Kinase 6Uterine Cervical NeoplasmsApoptosisAutophagyCell Line, TumorCell ProliferationFemaleGlycolysisHeLa CellsHexokinaseHumansMechanistic Target of Rapamycin Complex 1CDK6 protein, humanCyclin-Dependent Kinase 6HexokinaseMechanistic Target of Rapamycin Complex 1apoptosisautophagyCDK6Cervical carcinomaglycolysismTOR

Identifiers

PMID35167417
PMCPMC9037534
OpenAlexW4212961567

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.