Evidence map›Paper›PMID 35294319›Full record

ArticleBioengineered2022

LEM domain containing 1 (LEMD1) transcriptionally activated by SRY-related high-mobility-group box 4 (SOX4) accelerates the progression of colon cancer by upregulating phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway.

Ding Li, Ding Wang, Haofeng Liu, Xiaohui Jiang

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
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  10. MFNG is an independent prognostic marker for osteosarcoma.European journal of medical research · 2023
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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

4 authors at 2 institutions in 1 country.

Ding LiDepartment of Gastrointestinal Surgery, Affiliated Cancer Hospital of Nantong University, Nantong Cancer Hospital, Nantong City, Jiangsu Province, China.
Ding WangDepartment of Gastrointestinal Surgery, Affiliated Cancer Hospital of Nantong University, Nantong Cancer Hospital, Nantong City, Jiangsu Province, China.
Haofeng LiuDepartment of Gastrointestinal Surgery, Affiliated Cancer Hospital of Nantong University, Nantong Cancer Hospital, Nantong City, Jiangsu Province, China.
Xiaohui JiangDepartment of Gastrointestinal Surgery, Affiliated Cancer Hospital of Nantong University, Nantong Cancer Hospital, Nantong City, Jiangsu Province, China.
Nantong Tumor Hospital · CNNantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colon cancer is a highly malignant tumor in the digestive system. LEM domain containing 1 (LEMD1) is supposed to be a survival marker of poor prognosis in colon cancer. We aimed to explore the role and mechanism of LEMD1 in colon cancer progression. GEPIA database analyzed LEMD1 expression in colon cancer tissues and prognosis of colon cancer patients. LEMD1 expression in tumor cells was tested by RT-qPCR and western blotting. Proliferation of colon cancer cells was estimated by CCK-8 and colony formation assays. Transwell and wound healing assays were used to appraise the cell invasion and migration. Meanwhile, tube formation assays were used to evaluate angiogenesis. The possible binding sites between SRY-related high-mobility-group box 4 (SOX4) and LEMD1 were predicted by JASPAR database. Besides, SOX4 expression in colon cancer tissues and the correlation between SOX4 and LEMD1 were examined using the GEPIA database. Luciferase reporter and ChIP assays were used to verify the interaction between SOX4 and LEMD1. The expression of proteins in PI3K/Akt signaling was evaluated by western blotting. LEMD1 was overexpressed in colon cancer tissues and cells and associated with poor prognosis. Functionally, LEMD1 deficiency impeded the proliferation, migration, invasion and angiogenesis of colon cancer cells. Additionally, SOX4 had a positive correlation with LEMD1 and could bind to LEMD1 promoter. Rescue assays validated that SOX4 elevation reversed the suppressive role of LEMD1 deletion in the development of colon cancer and the expression of p-PI3K and p-AKT. Collectively, LEMD1 induced by SOX4 drove the progression of colon cancer by activating PI3K/Akt signaling.

Indexed as

Colonic NeoplasmsNeoplasm ProteinsSignal TransductionSOXC Transcription FactorsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktLEMD1 protein, humanNeoplasm ProteinsPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSOX4 protein, humanSOXC Transcription FactorsColon cancerLEMD1PI3K/Akt signaling pathwaySOX4

Identifiers

PMID35294319
PMCPMC9161920
OpenAlexW4221048412

What OpenQuestion holds

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LicenceCC BY
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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.