Target intelligence / Profile preview

HeLa cell viability

Molecular classification
Other, Cell line
01

Overview

HeLa cell viability refers to a phenotypic measure of the survival and proliferation of the HeLa immortalized cell line, which was originally derived from a cervical adenocarcinoma in 1951 (Masters, 2002, Nature Reviews Cancer). It is widely utilized in drug discovery as a cellular assay to evaluate the cytotoxicity or anti-proliferative effects of various chemical compounds (Scherer et al., 1953, Journal of Experimental Medicine). In databases such as ChEMBL, HeLa cell viability is categorized as a cell-line target rather than a specific molecular target like a receptor or enzyme (Gaulton et al., 2012, Nucleic Acids Research). The viability of these cells is typically assessed using metabolic indicators like the MTT assay or ATP bioluminescence, which reflect the overall health of the cell population (Riss et al., 2004, Assay Guidance Manual). Because HeLa cells harbor integrated Human Papillomavirus (HPV-18) DNA, they are particularly relevant for studying oncogenic processes and viral-host interactions (Adey et al., 2013, Nature). However, as a phenotypic endpoint, it does not provide information on a specific mechanism of action, as many different molecular pathways can influence cell survival.

Other names
HeLa cytotoxicityHeLa cell growth inhibitionHeLa cell proliferationHeLa survival
02

Mechanism of action

As a phenotypic endpoint, HeLa cell viability does not have a single mechanism of action; rather, it reflects the cumulative effect of drugs on various cellular processes such as DNA replication, microtubule assembly, and apoptotic signaling (Riss et al., 2004, Assay Guidance Manual).

03

Biological functions

Cell proliferationCell deathApoptosisMetabolism
04

Disease associations

CancerCervical cancerInfection
05

Safety considerations

Lack of molecular specificityHigh rate of false positives in phenotypic screensGenomic instability of HeLa cells leading to laboratory-specific variation (Masters, 2002, Nature Reviews Cancer)Poor translation from in vitro cytotoxicity to in vivo therapeutic efficacy
06

Interacting drugs

Paclitaxel

6 more in the full profile.

07

Biomarkers

ATP levelsMTT reductionLactate dehydrogenase (LDH) releaseCaspase-3 activityPropidium iodide staining

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