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LL/2 (LLC1)



Mus musculus


Doubling time: 21 hours (CLS). Caution: Could be identical to 3LL (CVCL_5653). Breed/subspecies: C57BL/6. DT Created: 04-04-12; Last updated: 06-09-19; Version: 22

Proper Citation

NCBI_Iran Cat# C587, RRID:CVCL_4358


Cancer cell line DT Created: 04-04-12; Last updated: 06-09-19; Version: 22


DT Created: 04-04-12; Last updated: 06-09-19; Version: 22


LL/2 (LLc1), LL/2(LLc1), LL/2, LL2, LLC1, LLC, Lewis lung carcinoma line 1, Lewis lung carcinoma, Lewis Lung Cancer, Lewis-Lung, Lewis Lung DT Created: 04-04-12, Last updated: 06-09-19, Version: 22



Cat Num


Cross References

BTO; BTO:0000181 CLO; CLO_0007325 CLO; CLO_0050167 CLDB; cl3208 AddexBio; C0016030/5000 ATCC; CRL-1642 BCRC; 60050 BCRJ; 0145 BioSample; SAMN11397632 CCRID; 3111C0001CCC000673 CCRID; 3131C0001000800007 ChEMBL-Cells; CHEMBL3307859 ChEMBL-Targets; CHEMBL614088 CLS; 400263/p546_Lewis-Lung ECACC; 90020104 IZSLER; BS TCL 216 KCB; KCB 200781YJ NCBI_Iran; C587 RCB; RCB0558 TKG; TKG 0153 TOKU-E; 2205 Wikidata; Q54902678 DT Created: 04-04-12; Last updated: 06-09-19; Version: 22


DT Created: 04-04-12; Last updated: 06-09-19; Version: 22

Originate from Same Individual

DT Created: 04-04-12; Last updated: 06-09-19; Version: 22

Twist1 Activation in Muscle Progenitor Cells Causes Muscle Loss Akin to Cancer Cachexia.

  • Parajuli P
  • Dev. Cell
  • 2018 Jun 18

Literature context:


Cancer cachexia is characterized by extreme skeletal muscle loss that results in high morbidity and mortality. The incidence of cachexia varies among tumor types, being lowest in sarcomas, whereas 90% of pancreatic ductal adenocarcinoma (PDAC) patients experience severe weight loss. How these tumors trigger muscle depletion is still unfolding. Serendipitously, we found that overexpression of Twist1 in mouse muscle progenitor cells, either constitutively during development or inducibly in adult animals, caused severe muscle atrophy with features reminiscent of cachexia. Using several genetic mouse models of PDAC, we detected a marked increase in Twist1 expression in muscle undergoing cachexia. In cancer patients, elevated levels of Twist1 are associated with greater degrees of muscle wasting. Finally, both genetic and pharmacological inactivation of Twist1 in muscle progenitor cells afforded substantial protection against cancer-mediated cachexia, which translated into meaningful survival benefits, implicating Twist1 as a possible target for attenuating muscle cachexia in cancer patients.

Funding information:
  • NIDDK NIH HHS - 2R01 DK-041274(United States)

LXR/ApoE Activation Restricts Innate Immune Suppression in Cancer.

  • Tavazoie MF
  • Cell
  • 2018 Feb 8

Literature context:


Therapeutic harnessing of adaptive immunity via checkpoint inhibition has transformed the treatment of many cancers. Despite unprecedented long-term responses, most patients do not respond to these therapies. Immunotherapy non-responders often harbor high levels of circulating myeloid-derived suppressor cells (MDSCs)-an immunosuppressive innate cell population. Through genetic and pharmacological approaches, we uncovered a pathway governing MDSC abundance in multiple cancer types. Therapeutic liver-X nuclear receptor (LXR) agonism reduced MDSC abundance in murine models and in patients treated in a first-in-human dose escalation phase 1 trial. MDSC depletion was associated with activation of cytotoxic T lymphocyte (CTL) responses in mice and patients. The LXR transcriptional target ApoE mediated these effects in mice, where LXR/ApoE activation therapy elicited robust anti-tumor responses and also enhanced T cell activation during various immune-based therapies. We implicate the LXR/ApoE axis in the regulation of innate immune suppression and as a target for enhancing the efficacy of cancer immunotherapy in patients.

Therapeutic potential of the phosphino Cu(I) complex (HydroCuP) in the treatment of solid tumors.

  • Gandin V
  • Sci Rep
  • 2017 Oct 24

Literature context:


[Cu(thp)4][PF6] (HydroCuP) is a phosphino copper(I) complex highly soluble and stable in physiological media that has been developed as a possible viable alternative to platinum-based drugs for anticancer therapy. HydroCuP potently inhibited the growth of human cancer cells derived from solid tumors by inducing endoplasmatic reticulum (ER) stress thus leading to cell death through paraptosis with a preferential efficacy against cancer rather than non-cancer cells. Aim of the present study was to assess the therapeutic potential of HydroCuP in vivo, in syngenic and xenograft murine models of solid tumors by triggering the Unfolded Protein Response (UPR) pathway. With respect to platinum drugs, HydroCuP induced a markedly higher reduction of tumor growth associated with minimal animal toxicity. In human colorectal cancer xenografts, chemotherapy with HydroCuP was extremely effective in both oxaliplatin-sensitive and resistant models. The favorable in vivo tolerability of HydroCuP was also correlated to an encouraging biodistribution profile. Additionally, no signs of drug-related neurotoxicity and nephrotoxicity were observed. Altogether, these results demonstrate that HydroCuP appears worth of further investigation to evaluate its therapeutic activity towards a broad spectrum of solid malignancies.

Funding information:
  • NCI NIH HHS - P30 CA014195(United States)