Evidence map›Paper›PMID 33117809›Full record

ArticleFrontiers in cell and developmental biology2020

STK35 Is Ubiquitinated by NEDD4L and Promotes Glycolysis and Inhibits Apoptosis Through Regulating the AKT Signaling Pathway, Influencing Chemoresistance of Colorectal Cancer.

Haojun Yang, Jie Zhu, Guangyao Wang, Hanyang Liu, Yan Zhou, Jun Qian

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed, 35 citations in OpenAlex.

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  7. Enhancing doxorubicin's anticancer impact in colorectal cancer by targeting the Akt/Gsk3β/mTOR-SREBP1 signaling axis with an HDAC inhibitor.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
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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

6 authors at 2 institutions in 1 country.

Haojun YangDepartment of Gastrointestinal Center, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, China.
Jie ZhuDepartment of Gastrointestinal Center, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, China.
Guangyao WangDepartment of Gastrointestinal Center, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, China.
Hanyang LiuDepartment of Gastrointestinal Center, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, China.
Yan ZhouDepartment of Gastrointestinal Center, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, China.
Jun QianDepartment of Gastrointestinal Center, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, China.
Nanjing Medical University · CNChangzhou No.2 People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of colorectal cancer (CRC) is often sporadic, but its etiology is multifactorial. Chemoresistance of CRC leads to tumor recurrence and poor prognosis in patients. The phosphorylation of protein kinase B (AKT) can activate metabolic reprogramming toward cellular glycolysis. Serine/threonine kinase 35 (STK35) regulates the cell cycle and is frequently associated with cancer progression, whereas little is known about its specific roles in CRC. In the current study, bioinformatics analyses were performed to investigate the relationship between STK35 and CRC prognosis. STK35 knockdown and overexpressing CRC cells were established to examine its functions in CRC. Fluorouracil (5-FU) was utilized to evaluate the effect of STK35 on CRC chemoresistance. Moreover, co-immunoprecipitation was performed to explore the ubiquitination of STK35. STK35 was highly expressed in CRC, and its protein expression was negatively correlated with the survival of CRC patients. Furthermore, STK35 overexpression could promote glycolysis, suppress apoptosis, upregulate p-AKT, and counteract the antitumor functions of 5-FU and neural precursor cell expressed developmentally downregulated gene 4-like (NEDD4L) in CRC cells. NEDD4L was associated with and could ubiquitinate STK35. STK35 could be a prognostic biomarker for CRC prognosis and has promotive effects on CRC cellular activities, partially through the AKT pathway. Moreover, STK35 also interferes with the chemosensitivity of CRC.

Indexed as

AKTapoptosiscolorectal cancerSTK35ubiquitination

Identifiers

PMID33117809
PMCPMC7578231
OpenAlexW3092292673

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.