The answer is yes, in laboratory experiments, and perhaps in a clinical setting as well.
Let me emphasize: the proof exists in controlled laboratory experiments. It has not been demonstrated to be true in human trials. So don't smoke up in the expectation that it's a better cancer treatment than a doctor's recommendations (generally chemotherapy, radiation therapy, or surgery, but would vary from patient to patient).
An article by Guzman in 2003 states that:
In addition, these compounds have been shown to inhibit the growth of tumour cells in culture and animal models by modulating key cell-signalling pathways. Cannabinoids are usually well tolerated, and do not produce the generalized toxic effects of conventional chemotherapies.
The question, at the time, is what the causal relationship is to inhibiting tumor growth. The answer to that question is apparently dependent on the type of cancer.
For instance, in prostate cancer, a metastudy (Ramos and Bianco, 2012) found that:
Prostate cancer cells possess increased expression of both cannabinoid 1 and 2 receptors, and stimulation of these results in decrease in cell viability, increased apoptosis, and decreased androgen receptor expression and prostate-specific antigen excretion.
In other words, cannabis causes increased prostate cancer cell death. They suggest that more study is warranted:
It would be of interest to conduct clinical studies utilizing cannabinoids for patients with metastatic prostate cancer, taking advantage not only of its beneficial effects on prostate cancer but also of their analgesic properties for bone metastatic cancer pain.
A similar story (Greenhough et al, 2007) appears to hold true in colorectal cancer:
... the mechanisms underlying the antitumoral effects of cannabinoids are incompletely understood, and evidence suggests these effects may be cell-type specific. Two signalling pathways that have been reported to be either positively or negatively regulated by cannabinoids (depending on the cell type and cannabinoid studied) are the RAS-MAPK/ERK pathway and the PI3K-AKT pathway. ... Here, we show, for the first time, that THC induces apoptosis in colorectal cancer cells, and that this occurs through the activation of the CB1 cannabinoid receptor. THC treatment resulted in the inhibition of both RAS-MAPK and PI3K-AKT survival signalling cascades
These two articles provide very specific pathways for cannabinoids to inhibit tumor growth and reduce existing tumor extent, but it's important to note that both are based on work in the lab. The call for bringing the prostate cancer work into more general therapeutic practice demonstrates that this is not, yet, a proven cancer therapy.