Evidence map›Paper›PMID 32157413›Full record

ArticleCancer chemotherapy and pharmacology2020

Involvement of ER stress and reactive oxygen species generation in anti-cancer effect of CKD-516 for lung cancer.

Soo Jin Kim, Kyung Hwan Jegal, Ji-Hye Im, Gyutae Park, Suntae Kim, Hye Gwang Jeong, Il Je Cho, Keon Wook Kang

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Article in Cancer chemotherapy and pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Thiazole, Isatin and Phthalimide Derivatives TestedCurrent medicinal chemistry · 2024
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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

8 authors at 4 institutions in 1 country.

Soo Jin KimCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, 08826, Republic of Korea.
Kyung Hwan JegalCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, 08826, Republic of Korea.
Ji-Hye ImCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, 08826, Republic of Korea.
Gyutae ParkCKD Research Institution, Chong Kun Dang Pharmaceutical Corporation, Yongin-si, Gyeonggi-do, 16995, Republic of Korea.
Suntae KimCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, 08826, Republic of Korea.
Hye Gwang JeongCollege of Pharmacy, Chungnam National University, Daejeon, 34134, Republic of Korea.
Il Je ChoDepartment of Herbal Formulation, MRC-GHF, College of Korean Medicine, Daegu Haany University, Gyeongsan, Gyeongsangbuk-do, 38610, Republic of Korea.
Keon Wook KangCollege of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, 08826, Republic of Korea. kwkang@snu.ac.kr.
Seoul National University · KRChong Kun Dang Bio (South Korea) · KRChungnam National University · KRDaegu Haany University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeCKD-516 (Valecobulin), a vascular-disrupting agent, inhibits microtubule elongation. We evaluated the effect of CKD-516 on lung cancer cells and the underlying molecular mechanisms.

methodsThe effects of S516, an active metabolite of CKD-516, were evaluated in HUVECs and three lung cancer cell lines and by a microtubule polymerization assay. Tubulin cross-linking was used to identify the binding site of S516 on tubulin, and Western blotting was performed to identify the intracellular pathways leading to cell death. Subcutaneous lung cancer xenograft models were used to assess the in vivo effect of CKD-516 on tumor growth.

resultsS516 targeted the colchicine binding site on β-tubulin. In lung cancer cells, S516 increased endoplasmic reticulum (ER) stress and induced reactive oxygen species (ROS) generation by mitochondria and the ER. In addition, CKD-516 monotherapy strongly inhibited the growth of lung cancer xenograft tumors and exerted a synergistic effect with carboplatin.

conclusionThe findings suggest that CKD-516 exerts an anticancer effect in company with inducing ER stress and ROS production via microtubule disruption in lung cancer cells. CKD-516 may thus have therapeutic potential for lung cancer.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBenzophenonesCell ProliferationEndoplasmic Reticulum StressHumansLung NeoplasmsMaleMembrane Potential, MitochondrialMiceMice, Inbred BALB CMice, NudeMitochondriaReactive Oxygen SpeciesTumor Cells, CulturedAntineoplastic AgentsBenzophenonesN-(4-(3-(1H-1,2,4-triazol-1-yl)-4-(3,4,5-trimethoxybenzoyl)phenyl)thiazol-2-yl)-2-amino-3-methylbutanamideReactive Oxygen SpeciesValineCKD-516ER stressMicrotubule disruptionROS

Identifiers

PMID32157413
OpenAlexW3012275464

What OpenQuestion holds

Textmetadata
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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.