Evidence map›Paper›PMID 25946136›Full record

ArticlePloS one2015

Let-7 Sensitizes KRAS Mutant Tumor Cells to Chemotherapy.

Xin Dai, Ying Jiang, Chalet Tan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Ovarian Cancer Susceptibility and Chemosensitivity to KRAS Modulation.International journal of molecular sciences · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. MicroRNA-143 replenishment re-sensitizes colorectal cancer cells harboring mutant, but not wild-type, KRAS to paclitaxel treatment.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    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

3 authors at 1 institution in 1 country.

Xin DaiDepartment of Pharmaceutical Sciences, Mercer University, Atlanta, Georgia, United States of America.
Ying JiangDepartment of Pharmaceutical Sciences, Mercer University, Atlanta, Georgia, United States of America.
Chalet TanDepartment of Pharmaceutical Sciences, Mercer University, Atlanta, Georgia, United States of America.
Mercer University Health Sciences Center · US

Funding

Functionalized Micellar Nanocarriers for Targeted Cancer TherapyR15CA152860 · NCI · MERCER UNIVERSITY MACON · PI TAN, CHALET · 2010 to 2010
$471k
NCI NIH HHS R15 CA152860NCI NIH HHS R15CA152860
6 · The paper itself

Abstract

KRAS is the most commonly mutated oncogene in human cancers and is associated with poor prognosis and drug resistance. Let-7 is a family of tumor suppressor microRNAs that are frequently suppressed in solid tumors, where KRAS mutations are highly prevalent. In this study, we investigated the potential use of let-7 as a chemosensitizer. We found that let-7b repletion selectively sensitized KRAS mutant tumor cells to the cytotoxicity of paclitaxel and gemcitabine. Transfection of let-7b mimic downregulated the expression of mutant but not wild-type KRAS. Combination of let-7b mimic with paclitaxel or gemcitabine diminished MEK/ERK and PI3K/AKT signaling concurrently, triggered the onset of apoptosis, and reverted the epithelial-mesenchymal transition in KRAS mutant tumor cells. In addition, let-7b repletion downregulated the expression of β-tubulin III and ribonucleotide reductase subunit M2, two proteins known to mediate tumor resistance to paclitaxel and gemcitabine, respectively. Let-7 may represent a new class of chemosensitizer for the treatment of KRAS mutant tumors.

Indexed as

Antineoplastic AgentsApoptosisCell CycleCell Line, TumorCell ProliferationCell SurvivalDeoxycytidineDrug Resistance, MultipleDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionExtracellular Signal-Regulated MAP KinasesGemcitabineHumansMCF-7 CellsMicroRNAsMutationAntineoplastic AgentsDeoxycytidineExtracellular Signal-Regulated MAP KinasesGemcitabineKRAS protein, humanMicroRNAsmirnlet7 microRNA, humanPaclitaxelPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins p21(ras)Ribonucleoside Diphosphate Reductaseribonucleotide reductase M2TUBB3 protein, humanTubulin

Identifiers

PMID25946136
PMCPMC4422443
OpenAlexW210871662

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.